1
TABLE OF CONTENTS
I. CONTACT INFORMATION 3
II. DISEASE PROCESSES & SURGICAL PROCEDURES
Transcatheter Aortic Valve Replacement (TAVR) 6
Cardiac: TAVR 9
Aortic Regurgitation 10
Mitral Valve Disease 12
Tricuspid Valve Disease 16
Coronary Artery Disease and CABG 17
Diseases Of The Aorta 19
Atrial Fibrillation (AF) 23
Hypertrophic Cardiomyopathy 24
Infective Endocarditis/ Root Abscess 27
Myocardial Bridge 29
Constrictive Pericarditis 31
Advanced Heart Failure: Ventricular Assist Device (VAD) 32
Heart Transplant 34
Extracorporeal Membrane Oxygenation (ECMO) 37
Lung Transplant 40
III. POST-OP MANAGEMENT
1. NEUROLOGIC
Delirium 44
Pain Control 45
Seizures 47
Spinal Cord Ischemia 50
Stroke / CVA 52
2. CARDIAC
Atrial Fibrillation & Electrolyte Replacement 53
Heart Blocks 57
Chest Pain 58
Pericardial Tamponade 59
Right Ventricular Failure 60
Systolic Anterior Motion (SAM) 62
Vasoplegia 62
Heart Failure 63
3. PULMONARY
Pneumothorax 65
Pulmonary Hypertension 65
Acute Respiratory Distress Syndrome (ARDS) 66
Atelectasis 68
4. GI
Acute Hepatic Dysfunction 69
Constipation And Illeus 71
GI Bleeding 71
Malnutrition (Tube Feeding/TPN) 73
5. GU/FEN
Acid Base Disturbances 74
Kidney Disease 77
Sodium Imbalances 79
2 Contact Information 3
6. HEMATOLOGY
Acute Blood Loss Anemia And Post-Operative Bleeding 80
TEG 83
Heparin Induced Thrombocytopenia (Hit) 84
Deep Vein Thrombosis 85
7. INFECTIOUS DISEASE
Sepsis 86
Cellulitis 88
Pneumonia 89
Urinary Tract Infection 91
8. ENDOCRINE
Acute Hyperglycemia And Diabetes Management 92
IV. PROCEDURES/DEVICES
1. PROCEDURES
Atrial Electrograms 97
Direct Current Cardioversion (DCCV) 97
Pacer Wire (PW) Removal 99
Rapid Sequence Induction 101
Bronchoscopy 103
2. DEVICES
IABP 103
Lumbar Drains 106
Temporary Pacemakers 106
On Q Pumps 109
Wound Vac 110
V. REFERENCE MATERIAL
Surgeon Preferences 112
Cardiac Surgery Procedure Clearance 114
1. PRE-OP
Check List 115
Cardiac Surgery Patient Blood Management Program 116
Obtaining Consent Procedure List 120
Periprocedural Anticoagulation Bridging 122
2. POST-OP
Imaging 123
ABG Interpretation 124
Advanced Hemodynamic Monitoring & Pulmary Artery Catheters 125
Common ICU Drips 127
Common PO Meds 128
Diagnosis Translation Examples 130
IICU Admission Requirements 131
INR Goals 132
Prophylactic Medications (GI, VA-PNA, DVT, Infection) 134
Supplemental O2 & Ventilator Management 134
Vad Bowel Regimen Protocol 138
End of Life Care 139
Patient Progression Checklist 140
Notes 141
PHONE NUMBERS
Emergency
Code Blue 211
Stroke Code 211
Transfusion STAT 3-6445
X-ray STAT 3-7030
Units
A31 Cardiac Clinic 1-8999
SAU 3-5163
ICU Team 1 650-206-3620 or 42829 *
8-9220
8-9218
ICU Team 2 1-6454*
6-7749
8-9223
North ICU Front Desk 3-6081
iICU Blue 650-850-1830
iICU Green 650-308-6625
iICU Float 650-304-9193
D3 Fax 650-725-4520
C1 5-8106
D1 CCU
D1 CSU
ED Unit Secretary
ED Charge RN
ED Triage RN
CDU
8-4662
4-2243
5-4492
4-1710, NP: 39904
OR Front Desk 3-7251
OR #8 5-7208
OR #9 5-7209
PACU 3-6631
Resident Desk-Falk 5-3832, 5-3835
Pharmacy/Lab
D3 Rx
D2 Rx
ICU Rx
B2 Rx
16777
55203
55923
36098
Core Lab 3-6111/3-8891
Micro Lab 4-4588/4-4589
Transfusion (Blood Bank) 3-6444
4 Contact Information Contact Information 5
Hillview Lab (HIT studies) 650-723-4813
Cytology 4-0077
TEG
Imaging
See page 123
Ancillary Sta
PT Scheduler 5-0299
Dialysis RN BAT phone 4-5350
PICC RN 6-8322
RT Supervisor 3-7709
3-6940
Chaplain 3-5151
E-29 Social Worker 650-701-5397
Admin
Admitting
Transfer Center
Bed Control (Rooming)
ANS (for beds)
3-6221
3-4696
3-5327 (part of transfer center)
6-1767
Central service supply 3-5047
Service Desk 3-3333
Food services 3-5538
Facilities 8-4400
Main Hospital
Page Operator 723-4000
723-6661, x288 in house
Security 3-7222
Human Resources 650-723-4748
Guest Services 8-3333
House keeping 8-4400
Medical Records 3-5721
Misc
Pager Numbers
Main Hospital page operator 723-4000, 723-6661, x288 in house
Department Pager #
Spanish Interpreter 17726
RT (Trach weaning) 17709
Nephrology Consult 24309
IR Consult, Body 27237
Urology 27155
Weekend CM 16292
Acute Pain 27150 (2-PAIN)
Psych Consult 15984
Wound RN 11003
EP NP 15590
IR NP (Line placement 35463 (3-LINE)
Neuro Critical Care 14061
Cardiac Surgery Consult 12182
Extensions
1- xxxx……..650-721-xxxx
3- xxxx……..650-723-xxxx
4- xxxx……..650-724-xxxx
5- xxxx……..650-725- xxxx
6- xxxx……..650- 736- xxxx
7- xxxx……..650- 497- xxxx
8- xxxx……..650-498- xxxx
6 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 7
AORTIC STENOSIS
Pathology:
hypertrophy and decreased LV compliance
Patients with LVH are at increased risk for subendocardial ischemia
Clinical Manifestations:
Angina
CHF symptoms (SOB, Edema)
Syncope
Physical Examination:
high pitched mid systolic crescendo-decrescendo murmur at the right upper
sternal border, which can radiate to the carotids, sternal notch, and apex
ejection click sometimes heard with a bicuspid aortic valve
Diagnostic Studies:
Echocardiogram:
Severity Grade
Indicator Mild Moderate Severe
Jet velocity (m/s) < 3.0 3.0 - 4.0 > 4.0
Mean gradient (mmHg) < 25 25 - 40 > 40
Aortic valve area (cm2/m2)
Cardiac catheterization: Allows for direct measurement of gradient by
crossing valve. If critical aortic stenosis, sometimes impossible to cross valve
with catheter
Indications for Surgery:
Presence of symptoms
Asymptomatic with any of the following:
presence of LV systolic dysfunction, LVH >15mm, and/or dilation
Vtach
LVH> 15 mm
AVA <0.6 cm squared, peak gradient > 50 mmHg
If undergoing surgery for another indication (ie CABG), and AVA <1.1 cm
squared
Preoperative Considerations:
Cardiac catheterization in anyone over age 40 or in younger patient with risk
factors, angina, or a positive stress test
If bicuspid aortic valve, CTA chest to evaluate for aortic root enlargement
Surgical Options:
Aortic valve repair or replacement via median sternotomy, minimally invasive,
or transcatheter (transluminal or transapical) approach. Bioprosthetic
valve conduit (CVG).
Postoperative Considerations:
Immediate post op Considerations:
volume replacement.
Use vasodilators as needed for HTN and to protect the suture line
Maintain NSR
Aspirin on all patients unless contraindicated
Mechanical valves require anticoagulation with Coumadin. Consider Heparin
op (see “INR Goals” reference chart on page 132)
TRANSCATHETER AORTIC
VALVE REPLACEMENT (TAVR)
Transfemoral Transapical
Approach: Approach:
Indications for Surgery:
AS > 1/0cm2/
<.05cm2/m
SYMPTOMS
NO SYMPTOMS
Evaluate for surgery
↓ LVEF/ LA >
4.5cm/ LV > 180g/
m2
Consider ???Co-Morbidty?
No
Yes
CATH
PFTs
CATH
PFTs
Dobutamine Stress
Echo
Fragility Assessment
PET for ischemic
Technical options
evaluation
Open AVR via Full
sternotomy or mini
Low risk
High Risk* Inoperable**
Vascular Access
Yes No
TF TAVR
TA TAVR
AS < 0.8cm2
+ VEL > 4m/s
Or gradiant > 40
TF AVI BAV
Apico-
Descending
* Currently defined as surgeon assessed >
15% risk of deat at STS > 8%
** Defined as > 50% risk of death or
irreversible serious post operative
mobidity as assessed by two surgeons
Indication for TAVR
References:
Up to Date, 2015
8 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 9
Approaches:
Transfemoral
Transaortic via small sternotomy
Potential Complications:
Stroke
Distal Embolization
Paravalvular Leak
Heart Block
Thoracic Aortic Dissection:
Local Vascular Injury
Local bleeding/hematoma
Inadvertent blockage of the coronary ostia.
Post-op Care/Considerations:
LVH and diastolic dysfunction
HTN
Especially concerning for transapical/transaortic approach.
First line agent Clevidipine
Conduction abnormalities
Higher risk with CoreValve, Evolut valves
removed by ICU team if no pacing required
May require PPM
AVOID ALL NODAL BLOCKING AGENTS IN THE POST OPERATIVE PERIOD
(no beta blockers, calcium channel blockers, digoxin, or amiodarone)
Anticoagulation:
Post-TAVR Antiplatelet and Anticoagulation Recommendations
Confidential – For Discussion Purposes Only
Post-TAVR Antiplatelet and Anticoagulation Recommendations
•P la vix 75 mg daily x 6 months post-TAVR
•ASA 81 m g daily indefinitely
•C o nsider ASA 81 mg alone if high bleeding risk or o ther
extenuating circumstance
No CAD
No AF
•Continue pre-TAVR anticoagulation regimen for AF
•No additional a ntiplatelet necessary
•C o nsider bridging with heparin or lovenox if high CVA
ris k
AF
•I f concomitant PCI with DES + TAVR, Plavix 75 mg daily
x 1 year minimum with ASA 81 mg indefinitely
•CAD +/- Remote PCI: Plavix 75 mg daily for a minimum
of 6 months (or min 1 year if recently post DES) and ASA
81 mg daily indefinitely
CAD
•Resume pre-TAVR anticoagulation regimen
•I f concomitant PCI with DES + TAVR, Plavix 75 mg daily
x 1 year with anticoagulation and no ASA necessary; if
no t on anticoagulation, then Plavix 75 mg daily for a
m inimum of one year and ASA 81 mg daily indefinitely
AF/CAD
Revised 2/10/16 MS/BF
• If there is concern about high risk for bleeding, discuss regimen with primary cardiologist before discharge
• If platelet count <100K, discuss with TAVR team
TAVR, CONTINUED
<1 cm2 and a mean aortic valve gradient greater than 40 mmHg or a jet velocity
greater than 4 meters a second.
TAVR work-up
Orders include:
CTA of chest, abdomen, and pelvis (TAVR protocol: includes Gated process,
evaluation of iliofemoral arteries with 3-D enhancement and measurements,
and Dr. Fleischman’s low dose contrast protocol)
Rationale: Annulus sizing: The aortic annulus is a complex 3-D structure.
It is a three-pronged coronet rather than a circular structure. It has three
anchor points at the nadir of each aortic cusp. CT provides reproducible
measurements of the annulus that provide a granular assessment of
aortic root geometry and annulus sizing. CT also reduces vascular access
complications and allows for assessment of luminal diameters, vessel
identify other high-risk features such as dissections and atheromas.
Transthoracic echocardiogram
Rationale: Recommended in the initial evaluation of patients with known
severity, assess hemodynamic consequences, determine prognosis, and
evaluate timing of intervention (AHA/ACC, 2014)
Coronary angiogram
Rationale: In the setting of AS, exertional dyspnea and chest pain may be
due to the combination of AS and CAD. Coronary angiogram with PCI alone
may resolve symptoms. (Ramee et al., 2016)
Pulmonary Function Testing
Rationale: In patients with AS evaluated for AVR, the STS risk score is
predominantly by PFT results. Even when lung disease is not suspected,
PFTs are abnormal in many patients undergoing AVR. Moderate/severe lung
disease, diagnosed predominantly by PFTs, is an independent predictor of
AVR. (Henn et al., 2016)
Objective Frailty
Rationale: Identifying frailty has important implications for clinical care.
The presence of frailty, worse health status, and more comorbid conditions
identify a subset of elderly patients at higher risk of dying during the follow-
Electrocardiogram
Rationale:
existing conduction abnormalities such as arrhythmias and heart block.
Common valves used at Stanford:
1. Medtronic: CoreValve Evolut R: Sheath delivered retrievable and
to higher incidence of heart block associated with this device, a temporary
2. Edwards Lifesciences: SAPIEN 3: A balloon expanded non-retrievable
ventricles is required to reduced turbulence prior to deployment of the valve.
Antiplatelet and anticoagulation considerations
of heart disease and the risk of thrombus formation on the new valve. Aspirin
81 mg a day and Plavix 75 mg a day is a standard regimen unless the patient has
a condition that precludes it, e.g., GI bleeding. If a patient is already taking an
10 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 11
condition and to prevent valve thrombus. Please review full guideline posted in
your department.
Please see below for which meds pre-TAVR should be held and when.
Of note, Plavix and ASA should still be ordered for morning of surgery on TF
patients when they are on C1.
THV Pre-procedure Medication Guideline
Medications to hold TransFemoral (TF) TransApical (TA) TransAortic (TAo)
Warfarin (lovenox
ridging per MD’s
discretion)
Hold 5 days before Hold 7 days before Hold 7 days before
Pradaxa Hold 4 days before Hold 4 days before Hold 4 days before
Eliquis Hold 48h before Hold 48h before Hold 48h before
Xarelto Hold 48h before Hold 48h before Hold 48h before
Eient Continue Hold 7 days before Hold 7 days before
Plavix Continue Hold 7 days before Hold 7 days before
Ticagrelor Continue Hold 7 days before Hold 7 days before
Oral Diabetic
Medications
Hold Metformin 48 hours before the procedure. Hold all other oral
diabetic medicine the morning of the procedure.
Insulin Take half of the evening dose. Hold the morning of the procedure.
Nodal blocking
agent
Ca Channel
blockers
Beta Blockers
Cardiac glycoside
(Digoxin)
Amiodarone
Clonidine
Hold the morning of the procedure.
AORTIC REGURGITATION
Pathology:
aortic root dilation, or ascending aortic dissection.
which over time will contribute to decreased ejection fraction.
Clinical Manifestations:
CHF symptoms
Physical Examination:
Early diastolic decrescendo murmur at LUSB. Increased with leaning forward
and expiration
Diagnostic Studies:
Echocardiogram:
AR Grading Central Jet
width*
Regurgitant
Volume (per
beat)
EROA (eective
Regurgitant
oriace area)
Mild < 25% of LVOT
width
< 30mL <0.1cm2
Moderate 25-65% of LVOT
width
30-59mL 0.1-0.3cm2
Severe >65% of LVOT
width
>60mL >0.3cm
Indications for Surgery:
For severe Chronic AR:
Chronic Severe Mitral
Regurgitation
Clinical
Evaluation =
Echo
Symptoms? No Yes
LV Function LV Function
Normal LV
Function
EF > 60%
ESD < 40mm
LV Dysfunction
EF < 60%
and/or
ESD > 40mm
EF > 30%
ESD < 55mm
EF <30 %
and/or
ESD > 55mm
New Onset Afib?
Pulmonary HTN?
Class I
Class I
MV Repair,
If not possible
MVR
Chordal
preservation
likely?
Yes
No?
Medical
therapy
Yes
No
MV repair
likely?
Class
IIa
Class
IIa
No? Clinical
eval/Echo every
6 months
Yes
Class
IIIA
Reference:
Nishimura, et. al. (2014). A Report of the American
College of Cardiology/American Heart Association Task
Focus on Practice Guidelines. AHA/ACC Valvular heart
disease guidelines, page 487.
For Mild to Moderate AR:
LV dysfunction or dilation
Symptoms only is not an indication to operate
Endocarditis with hemodynamic compromise or embolic events
If undergoing surgery for another indication, valve replacement is indicated
for anything greater than mild AR
Preoperative Considerations:
Control hypertension. Avoid bradycardia.
Intra-aortic balloon pump is contraindicated
Surgical Procedures:
Aortic valve repair or replacement via median sternotomy or minimally
invasive approach.
Bioprosthetic or mechanical valve.
If AR due to root dilatation
Valve sparing aortic root replacement (Tirone David)
Postoperative Considerations:
Immediate post op Considerations:
secondary to dilated LV
Maintain NSR
12 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 13
Aspirin on all patients unless contraindicated
Mechanical valves require anticoagulation with Coumadin. Consider Heparin
op. (see “INR Goals” reference chart on page 132)
References:
Otto, C.M., Gaaasch, W.H, Yeon, S.B. (2016). Clinical manifestations and diagnosis of aortic stenosis in
adults. Up to Date.
MITRAL VALVE DISEASE
Mitral Stenosis (MS):
3.
4.
pulmonary hypertension and subsequently right ventricular failure and
tricuspid regurgitation.
5. Causes:
•
Rheumatic valve disease; most common cause (causes thickening
and shortening of the chordae tendineae).
•
common in older patients or those exposed to heavy radiation
treatment), Congenital Mitral Valve deformities, Carcinoid syndrome,
Mitral Regurgitation/Insuiciency (MR):
1. Acute MR
•
which may lead to acute pulmonary edema and cardiogenic shock
•
Causes: Papillary muscle rupture/ischemic injury, endocarditis, chordae
rupture
2. Chronic MR
•
decreased LA/LV compliance.
•
Causes:
i.
1. Rheumatic fever, ruptured chordae tendineae or chordae elongation,
annular dilatation, focal myocardial dysfunction
is thickened, complex MR
syndrome, or an ostium primum ASD)
ii. Functional Disease (Secondary MR): not due to valve itself, but
dysfunction of structures that hold valve
2. Mitral valve prolapse (MVP):
allowing a small amount of blood to leak backward
b. Causes: myxomatous degeneration, Barlow’s syndrome, Marfan’s
syndrome, and rheumatic heart disease
iii. Infective Endocarditis
iv. Ischemic Cardiomyopathy
v.
Clinical Manifestations, Diagnostic Studies/ Classication
Echo: test of choice for diagnosis
Mitral Valve Echo Values
MS grading Valve Area Mean gradient Pulmonary
artery pressure
(mmHg)
Mild >1.5 cm2 <5mmHg <30mmHg
Moderate 1.0-1.5 cm2 5-10mmHg 30-50mmHg
Severe <1.0cm2 >10mmHg >50mmHg
MR grading Jet area Regurgitant
Volume
EROA (eective
Regurgitant
oriace area)
Mild <20% of LA area <30mL <0.2cm2
Moderate 20-40% of LA area 30-59mL 0.2-0.39
Severe >40% of LA area >60mL >0.40cm2
MS:
Murmur: Loud S1, opening snap, diastolic low-pitched rumble/murmur
best heard at the apex
14 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 15
MR:
pan-systolic murmur, sometimes a late-systolic murmur, best heard at
Indications for Surgery:
MS:
Severely symptomatic patients (NYHA class III or IV) with severe mitral
Patients who have failed previous percutaneous balloon mitral
commissurotomy
MR:
Chronic Severe Mitral
Regurgitation
Clinical
Evaluation =
Echo
Symptoms? No Yes
LV Function LV Function
Normal LV
Function
EF > 60%
ESD < 40mm
LV Dysfunction
EF < 60%
and/or
ESD > 40mm
EF > 30%
ESD < 55mm
EF <30 %
and/or
ESD > 55mm
New Onset Afib?
Pulmonary HTN?
Class I
Class I
MV Repair,
If not possible
MVR
Chordal
preservation
likely?
Yes
No?
Medical
therapy
Yes
No
MV repair
likely?
Class
IIa
Class
IIa
No? Clinical
eval/Echo every
6 months
Yes
Class
IIIA
Reference:
Nishimura, et. al. (2014). A Report of the American
College of Cardiology/American Heart Association Task
Focus on Practice Guidelines. AHA/ACC Valvular heart
disease guidelines, page 487.
Mitral Stenosis
Symptomatic Asymptomatic
MVA >/=
1.5cm2
Exercise
Moderate to
Severe MS
MVA < 1.5cm2
PASP > 60mmHg
PAWP >/= 25
No
Yes
Moderate to
severe MS
MVA < 1.5cm2
Mild MS
MVA >/= 1.5cm2
Medical
Management
Follow up every
12 months
Favorable
Morphology?
No
Yes
PSAP > 50mmHg?
Yes
Investigation of
possible other
source of
symptoms
Consider PBMV
(exclude LA
clot, 3-4+ MR)
Favorable
Morphology
No
No
Consider
MVR/MV
Repair
MVA= mitral valve area
PMV = percutaneous mitral balloon valvotomy
PASP = pulmonary artery systolic
PAWP= pulmonary artery wedge pressure
Surgical Procedures:
1. Repair is preferred over replacement
2. Replacement (bioprosthetic or mechanical valve):
i. Indications for replacement over repair:
3. Surgical approaches:
i. Median Sternotomy
ii. Mini-Sternotomy
iii. Minimally Invasive via Right Thoracotomy and groin cannulation
Intra Op Considerations:
When performing concomitant coronary bypass, the distal anastomoses are
completed before mitral valve intervention
When performing concomitant aortic valve replacement, the aortic valve
cutting of mitral annular sutures. Then the mitral procedure is performed
before the aortic valve replacement.
When performing concomitant tricuspid valve surgery, a trans-septal
(Sellke & del Nido & Swanson; chap 80
Minimally Invasive Mitral: consider size and presence of calcium in femoral
artery for cannulation; consider calcium in descending aorta for cannulation
Post op considerations:
Immediate Post-op Considerations:
For MS:
Maintain NSR
pressures vary with degree of pre-existing pulmonary hypertension
diuresis
For MR:
Maintain NSR
Resolution of MR leads to increased LV wall stress leading to LV
Adequate volume resuscitation and inotropic support may be
required. Be cautious with volume resuscitation in patients with RV
dysfunction.
Closely monitor RV function especially in patients with pre-existing
pulmonary hypertension. Inotropic support, pulmonary vasodilators,
and diuresis may be required.
following MVR. Ensure adequate preload and avoid hypotension with
the use of vasoconstrictors as necessary. Avoid inotropes.
Systolic anterior motion (SAM) that produces LVOTO may be present
following mitral valve repair. Management same as LVOTO.
Minimally Invasive Mitral: REMOVE SUTURE
POD #3
ASA unless contraindicatesd
Mechanical valves require anticoagulation with
Coumadin. Bridge with heparin drip.
Mechanical valves in mitral position require higher
See “INR Goals” reference chart on page 132)
References:
Sabiston, D. C., Sellke, F. W., J., D. N., & Swanson, S. J. (2010). Sabiston & Spencer surgery of the chest.
Philadelphia: Saunders/Elsevier.
16 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 17
TRICUSPID VALVE DISEASE
Etiology & Pathology
TS (tricuspid stenosis) is rare, usually develops as a result of rheumatic
disease or associated with mitral stenosis
TR (tricuspid regurgitation) is usually “functional” in nature. Occurs as a
complication of mitral valve disease causing pulmonary hypertension, RV
dilation, and tricuspid annular dilation. A small degree of TR is present is
almost 70% of normal adults.
A common cause of TR is endocarditis (usually caused by IV drug abuse, an
indwelling pacemaker wire, or hemodialysis catheter)
Clinical Manifestations
Fatigue
With severe disease, right heart failure symptoms may be present (right
abdominal pain, shortness of breath, swelling in legs or abdomen)
Physical Exam
Systolic murmur that increases with inspiration, prominent jugular
pulsations, and occasionally a pulsatile liver.
Diagnostic Studies/Classication (Via Echocardiogram)
Signicant tricuspid stenosis
Mean pressure gradient >/= 5mmHg
Tricuspid
Regurgitation
MILD MODERATE SEVERE
Jet area < 5 5-10 >10
RV/RA/IVC Size Normal Normal or dilated Usually dialates
Indications for Surgery
Tricuspid stenosis: Surgery is indicated for class III-IV symptoms including
hepatic congestion, ascites, and peripheral edema that are refractory to salt
restriction and diuretics.
Tricuspid Regurgitation:
Class I: TV repair is indicated when severe TR is present with mitral valve
disease requiring mitral valve surgery
Class II: TV repair or replacement is reasonable for symptomatic, severe
primary TR.
Class III: TV repair is reasonable is less than severe TR is noted at the time of
mitral surgery, but pulmonary hypertension or dilated tricuspid annulus is
present.
Persistent sepsis or recurrent pulmonary embolization from tricuspid valve
vegetation is an indication for surgery
Class III: surgery should NOT be considered in asymptomatic patients with a
PA pressure <60 and no mitral valve disease
Surgical Procedures
Tricuspid commissurotomy can be performed for rheumatic TS
Tricuspid ring annuloplasty with a ring or suture technique is feasible and
preferred for the majority of patients with functional TR
coaptation prevent an annuloplasty technique from eliminating the TR.
Intra op & Post op Considerations
During TV repair, sutures are placed near the conduction system, thus
patients are more likely to develop heart block. If there are concerns that
permanent pacing may be required, epicardial pacing leads should be placed
TVRepair surgery)
ASA unless contraindicated
Mechanical valve requires anticoagulation with Coumadin (See “INR Goals”
reference chart on page 132)
References:
Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
CORONARY ARTERY DISEASE AND CABG
Pathophysiology:
but typically occurs at points of turbulence (e.g., vessel bifurcations)
Risk Factors for atherosclerotic coronary artery disease: hypertension,
smoking, high LDL, low HDL, obesity, diabetes, family history.
Clinical manifestations:
CAD manifested by MI, angina, or CHF
Angina (stable vs unstable)
Stable angina = chest pain that occurs predictably and is reproducible
18 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 19
CCS Functional Classication of Angina
Class Description
Class I Angina only during strenuous or prolonged physical activity
Class II Slight limitation, with angina only during vigorous physical activity
Class III Symptoms with everyday living activities
(i.e. moderate limitation)
Class IV Inability to perform any activity without angina or
angina at rest (i.e. severe limitation)
Physical Exam:
Diagnostic studies:
Cardiac catheterization is the gold standard for diagnosing CAD
Myocardial perfusion scan
Echocardiogram
Stress testing
Indications for surgery:
Presence of 3 vessel disease (especially if EF < 40%)
Presence of 2 vessel disease with 70% stenosis of LAD
Surgical procedures:
(LIMA to LAD) is the single most important determinant of long-term
and event-free survival for patients who have undergone CABG
Traditional on pump CABG (via median sternotomy)
Conduit choice:
Arterial: LIMA (1st choice), RIMA, Radial artery via endoscopic harvest
Venous: Greater Saphenous Vein via Open or endoscopic vein harvest
Consider for high risk patients (> 70 years old, CKD, increased risk stroke
or carotid stenosis)
Minimally invasive direct coronary artery bypass (MIDCAB)
LIMA to LAD only
LIMA is harvested endoscopically though three small ports placed in the
through which the LIMA to LAD anastomoses is constructed via direct
vision
to remaining lesion by interventional cardiologist
Preoperative Considerations:
All patients with CAD must take beta blocker within 24 hours of induction for
surgery (or document why contraindicated)
narrowing/steal which precludes the use of the LIMA, diagnosed with carotid
ultrasound.
IF L radial pulse <2+ or faint compared to R, needs testing
Carotid ultrasound for those with history of prior CVA
Radial artery harvest work up for those < 70
Vein mapping (previous vein stripping, CABG, diabetes)
Post-operative Considerations
Immediate post-operative care:
If EVH or RAH completed, ACE wrap to extremity for 24 hours post op
ASA unless contraindicated
Beta blocker and statin therapy initiated prior to discharge (or document why
contraindicated)
References:
Cutlip, D., Levin, T., Aroesty, J.M. (2016) Revascularization in patients with stable coronary artery disease:
DISEASES OF THE AORTA
Denitions
Aortic aneurysm – localized dilation (> 50% increase in diameter) of the aortic
wall
Aortic dissection – intimal tear of the aorta separating intima from the medial
layers and creating a false lumen
Aortic intramural hematoma (IMH) – hematoma within the medial layer of the
aorta that occurs when the vasa vasorum ruptures. Does not involve intimal
tear.
Penetrating atherosclerotic aortic ulcer (PAU) – atherosclerotic ulcer that
penetrates through the intima layer of the aorta and dissects into the median
wall and forms a pseudoaneurysm.
Risk Factors
Atherosclerosis
Hypertension
Connective tissue disorders (i.e. Marfan, Loeys-Dietz, Ehler’s-Danlos syndrome)
Drug abuse (cocaine, meth)
Trauma: blunt, IABP, cardiac or aortic surgery, cardiac catheterization
Bicuspid aortic valve
Aortitis (ie giant cell arteritis)
Pregnancy
Clinical Manifestations
ripping, chest pain that radiates to the back
ischemia
20 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 21
Physical Exam
Note carotid, radial, and
femoral pulses bilaterally
Change in neurological status indicating compromise of cerebral perfusion
Abdominal pain indicating bowel ischemia
Dissection Classications:
Type I – Dissection originates in the ascending aorta and may extend
down to the descending aorta and/or abdominal aorta
Type II – Dissection is limited to ascending aorta only
Type III – Dissection originates in the descending aorta and extends to
just above the diaphragm (type IIIa) or below the diaphragm (type IIIb)
Type A – Dissection originates in ascending aorta and may extend into
descending aorta
Type B – Dissection originates in descending aorta however may
retrograde into the aortic arch
Aneurysm Classications:
extends to the celiac axis and mesenteric arteries
Type II – Dissection includes type 1 but extends into infrarenal aorta
Type III – Dissection originates in the lower descending thoracic aorta
and involves remainder of the aorta
Type IV – Dissection originates at the diaphragm and involves the entire
abdominal aorta
Management
Inpatient/ICU Care:
Obtain blood pressure in both arms.
Insert arterial line in right arm
Control heart rate and blood pressure
otherwise)
otherwise)
Manage pain
Follow up with surgical team regarding whether or not acute surgical
intervention is indicated
Acute type A aortic dissections are always a surgical emergency.
Uncomplicated type B dissections are medically managed
Outpatient care:
BP control
No burst activity/exercise requiring Valsalva
Follow up:
Expansion rate ~0.1cm/yr for TAA, ~_.4cm/yr for AAA
Screening for CAD, PAD, Aneurysm elsewhere, esp popliteal. 25% of pts
with TAA Will also have AAA.
Surgical indications for Aortic Aneurysms:
of note, when looking at aortic measurements, must consider ASI (aortic size index,
relation of height and weight to maximum aortic diameter)
TAA growing > 1cm/yr
Ascending > 5.5cm; descending >6cm.
Marfan’s/Loey Dietz patient > 4.5-5cm
For any aneurysm > 4cm if planning for AoV surgery
Other Surgical Triggers:
4.5 cm in the setting of a family hx positive for rupture or dissection
5.0 cm with moderate or worse aortic valve disease
Primary failure of aortic valve (AS/AI)
Surgical indications for Aortic Dissections
Type A: emergent surgery indicated in all acute type A dissections as well
as chronic type A
Type B: usually treated medically. Endovascular or surgical repairs in
complicated patients with chronic pain, uncontrolled hypertension,
evidence of aneurysmal expansion or rupture, or vascular compromise
Surgical intervention
OPEN REPAIR
Ascending aortic dissection/aneurysm: aortic valve repair/replacement,
place valve conduit. If tear extends across arch, may replace entire arch
Descending aortic dissection/aneurysm:
replacement.
Intra-operative considerations
DHCP: deep hypothermic circulatory arrest
Used when aorta cannot be clamped to perform aortic anastomosis
Patient is cooled for neuroprotection
SACP: selective antegrade cerebral perfusion
arrest to perfuse brain
RCP: retrograde cerebral perfusion
Cold, oxygenated blood into SVC to maintain cerebral hypothermia
Extensive cooling and rewarming is associated with coagulopathy and
bleeding
Neurologic recovery may take up to 24 hours
Decadron, mannitol and or Lasix may also be given for neuroprotection
22 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 23
Cross-clamping of the distal aorta can result in paraplegia or renal failure
(Reference: section 3 post-operative management of spinal cord ischemia)
MINIMALLY INVASIVE REPAIR
Endovascular stenting for complicated type B via TEVAR
i.
ii. On pre-op CT, look for communication between the true and false lumen
to help determine what areas can be safely stented.
iii. It is also important to look at the diameter of the femoral vessels to
determine whether access needs to be gained higher than the groin
(typically accessed somewhere near the level of the belly button or
slightly lower).
iv. Indications for TEVAR
a. Asymptomatic patients with thoracic aortic aneurysms
b. Patients with descending thoracic aortic aneurysms that is at least
2 times greater than the adjacent aorta, measuring at least 5cm.
of the aneurysm in order to
aortic walls.
c. Patients that are elderly and/or in poor overall health and would be
unlikely to survive an open operation
d. Can be used in chronic or acute dissections
v. Contraindications for TEVAR
a. Symptomatic patients – those with symptoms typically require open
repair of TAA
b. Patients with access vessels less than 8mm or vessels that are tortuous.
(patients that do not have 2cm of suitable aortic dimension on either
side of the aneurysm).
d. Patients who have branch vessels that will be occluded by the stent-
e. Patients with connective tissue disorders such as Marfan’s in which it is
expected further tissue degeneration may occur.
Postoperative Management
Blood pressure management:
Must balance risk of expansion of residual dissection/aneurysm (if
present) with risk of end organ/spinal cord ischemia
Establish hemodynamic goals with CT Surgery attending and ICU team
Monitor for bleeding and correct coagulopathy
Neuro monitoring:
Q1H Pupillometry for patients who underwent circulatory arrest
Lumbar drain: placed preoperatively for patients undergoing descending
aorta repair at high risk for paraplegia (for more detail, see Reference: Post-
operative management: Spinal cord ischemia; Devices: Lumbar drains).
perfusion pressure >80mmHg
exam intact
Monitor for end organ ischemia:
Trend UOP
Serial lactate, BMP, LFT, SvO2
References
Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
ATRIAL FIBRILLATION (AF)
Pathology:
rapid rates, producing an exceedingly rapid, erratic rhythm.
Post-operative atrial brillation: occurs in 30-40% of post op cardiac
Clinical manifestations:
Can be asymptomatic
Fatigue, palpitations, dyspnea, lightheadedness, chest pain
Physical Exam:
Discrepancy between auscultated heart rate and palpable pulse rate (minimal
Diagnostic Studies:
12-lead EKG:
Disorganized atrial activity between QRS complexes occurring in an irregular
pattern. RVR = rapid ventricular response HR> 150bpm
Classication
New onset 1st detected vs reoccurrence > 2 episodes
Paroxysmal
within 7-days or spontaneously
Persistent
with cardioversion
Permanent/ Chronic
or no plans for cardioversion
Secondary Caused by a separate underlying condition:
MI, cardiac surgery, pulmonary disease.
Lone atrial brillation Age < 60; no clinical or echocardiographic reasons
are found
Non-valvular Not caused by valvular disease, prosthetic heart
valves, or valve repair
Risk of stroke from atrial brillation – calculated with CHA2DS2VASc score.
CHADS2 VASc Score (>2 pts equals indication for anticoagulation)
C (1)
H (1) Hypertension
A (2) Age >74 years old
D (1) DM
S (2) Prior stroke or TIA or thromboembolism
V (1) Vascular disease (PAD, MI)
A (1) Age 65-74 years old
S (1) Sex category female
Indications for Surgery
advanced disease patients
who have failed prior catheter ablations
24 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 25
Cox Maze procedure: can be performed for patients with non paroxysmal
replacement, CABG)
Surgical Procedures
Atrial Fibrillation Treatment Options
Medication
Therapy
(Drugs)
Direct Current
Cardioversion
(Shock)
Catheter Ablation
Typically used to treat:
1. Paroxysmal atrial fibrillation
2. Duration < 1 year
3. Left Atrium size < 4.0cm
Hybrid Ablation
CATHETER + SURGERY
Typically used to treat:
1. Non-paroxysmal atrial fibrillation
2. Average Duration ~ 4 years
3. Average Left Atrium size ~ 4.5cm
Cox Maze Procedure
Typically used to treat:
1. Non-paroxysmal atrial fibrillation
2. Average Duration ~ 6.5 years
3. Left Atrium size > 5.0cm
“Internal Ablation”
Completed by
Electrophysiologist
LEAST INVASIVE MOST EFFECTIVE
“Open heart surgery”
Requires heart lung-
bypass machine
Part 1: “External
Ablation”
Completed by
Cardiac Surgery
Part 2: “ Internal
Ablation”
Completed by
Electrophysiologist
Performed
by Cardiac
Surgeon
(Dr. Lee)
“Minimally Invasive”
Bilateral video assisted
thoracospic (VATS)
My information
TYPE: _______________
DURATION: ___________
LA SIZE:_______________
Anson M. Lee, MD
Assistant Professor of Cardiothoracic Surgery (Adult
C
ardiac Surgery) at the Stanford University Medical Center
Internal &
External Ablation
Completed by
Cardiac Surgeon
Anterior Thoracotomy Incision
Traditional Sternotomy
Incision
Video Assisted Thoracoscopic Surgery (VATS)
Incision
Post-operative considerations:
heart surgery
All patients will need to resume home antiarrhythmic agents and
anticoagulation (regardless of rhythm)
Only consider DCCV for post op Maze patients if unstable or rate is very fast
will be in NSR at 1 year post operatively.
Consider starting Inspra (Aldactone) 25mg PO BID, once creatinine,
potassium, and blood pressure will tolerate and continue on discharge.
Reference:
Bojar, Robert, M., (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
Am Fam Physician. 2011;83(1):61-68. American Academy of Family Physicians.
Lawrance, Christopher P. (2015) Curr Opin Cardiol. January: 30(1): 58-64.
Pison MD, Laurent, La Meir MD PhD, Mark, Crijns MD PhD, Harry. (2013) Journal of Atrial Fibrillation
Vol-6; Issue2: 49-56.
HYPERTROPHIC CARDIOMYOPATHY
Etiology
HCM is the most common genetic cardiac disease, occurs in ~ 1/500 young
adults
ie HTN or valvular
aortic stenosis)
Pathology
In the obstructive form of HCM (~70% of patients w/ HCM), septal hypertrophy
and abnormal SAM of the MV produce LVOT obstruction and variable degrees
of MR
SAM is the abrupt anterior motion of the mitral valve in which the
le ventricular outow tract obstruction (LVOTO)
Consider SAM in setting of worsening hypotension with increased
inotropic support
intraventricular septum, papillary muscle displacement, and
SAM of the mitral valve may also be present secondary to mitral valve
repair
LVOT obstruction produces markedly increased intraventricular
pressures thereby increasing myocardial wall stress and oxygen
demand
coaptation
Diastolic dysfunction with increased LVEDP (dependent on atrial contraction)
Clinical manifestations
Syncope
Dyspnea (LV diastolic dysfxn/ MR)
Fatigability
Angina
Important History Questions:
History of vtach/ cardiac arrest? AICD?
Family Hx sudden cardiac death
Has genetic testing been performed? If so are they positive for gene?
Physical Exam
Systolic murmur @ LSB (can radiate across precordium), standing/
Crescendo-decrescendo peak mid-late S1, end before S2
MR may produce separate holosystolic murmur at apex
4th heat sound if LVH
26 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 27
Diagnostic Studies
Echo:
Presence of SAM? MR? If MR, dilated LA?
Dx of HCM based on LVOT gradients: (rest, Valsalva, peak exercise)
peak gradient @ rest > 50 + symptoms (not improved w/ med therapy)
(others say resting gradient as low as 30 mmHg)
peak gradient @ rest > 80 + asymptomatic
Stress/Exercise- induced gradient >100mmHg
Exercise Stress Echo
BP response: should increase >20 mmHg w/ exercise or pt @ higher risk
for SCD
If no delayed gadolinium enhancement (DGE), means no scarring, likely
don’t need ICD if no history of VT
thick)
CATH:
Pulm HTN (RVSP > 35) in 50%, severe ( >50) in 17% patients
Surgical Indications:
Septal thickness >18mm
Atypical septal morphology
Surgical Procedures
1. Septal Ablation (done in cath lab by interventional Cards)
myocardial infarction within the proximal ventricular septum
Leads to progressive thinning and reduction of the LVOT obstruction
2. Septal Myotomy/Myectomy with possible MV repair/replacement
Considered “gold standard” for the treatment for HCM patients refractory to
optimal medical therapies
Surgical procedure that relieves the LVOT obstruction by resection of a small
portion of muscle from the basal septum in order to
obstruction
Some patients may also require mitral valve repair if they also demonstrate
systolic anterior motion (SAM) of the mitral valve that is also contributing the
LVOT obstruction.
Benet of surgical intervention vs. ablation:
SURGERY: resultant lower gradient and less requirement for post-op PPM
creates “mush-like” infarcted tissue
Pre- op considerations
Pre-load dependent (gradient worse if dehydrated)(Avoid Jacuzzis; Avoid
lasix/diuretics)
AVOID inotropes
Dual-chamber pacing with a short AV delay (or V-pacing) to ensure complete
approximately 35%. Septal dyssynchrony may actually pull septum out
of LVOT
Intra-op considerations
95% cases don’t require MV repair if septum adequately excised (SAM will
improve w/ myectomy alone)
RISKS: Need for PPM (can’t see bundle His/ looks like muscle)
Post op considerations
caution
Avoid inotropes if possible
Avoid tachycardia (HR 60-80)
slow-normal HR)
If no ICD pre-op & plan to place prophylactic ICD post-op (if risks for sudden
cardiac death (SCD))
Reference:
Bojar, Robert, M., (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
Indian Journal of Anaesthesia, Vol. 58, No. 1, January-February, 2014, pp. 51-54
INFECTIVE ENDOCARDITIS/ ROOT ABSCESS
Etiology
Native valve endocarditis is most commonly caused by Streptococcus
viridans, Staphylococcus aureus, or coagulase-negative staph.
Tricuspid valve endocarditis is usually caused by IV drug abuse
Incidence of prosthetic valve endocarditis is approximately 0.5-1% per
patient-year. Most common cause is by staph organism
Pathology
myo-cardial tissue, systemic embolization of valve vegetations, or persistent
systemic sepsis.
Embolization is more common with mitral valve involvement, staphylococcal
organ-ism, and large or mobile vegetations.
Clinical manifestations
Presence of moderate to severe congestive heart failure maybe present from
re-gurgitant lesions.
28 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 29
pulmo-nary hypertension
Complete heart block: More common in aortic valve endocarditis or annular
ab-scess
Physical Exam
Splinter hemorrhages, Osler’s nodes may be present
Diagnostic Studies/ Classication
TEE (transesophogeal echocardiogram) is gold standard for identifying
echocardiogram) in identi-fying and quantifying the size and mobility of
the vegetations, detecting annular destruction, and identifying valvular
abnormalities.
Coronary angiography should be avoided, if possible, if mobile aortic valve
Duke Criteria:
Dente Infective Endocarditis is established in the presence of any of the
following:
Pathologic criteria Pathologic lesions: vegetation or intracardiac abscess
demonstrating active en-docartitis on histology
Microorganism: on culture/histology of a vegetation or
intracardiac abscess
Clinical criteria
(See major & minor
clinical criteria under
References)
2 major clinical criteria OR
1 major and 3 minor clinical criteria OR
5 minor clinical criteria
Possible Infective endocarditis
Presence of 1 major and 1 minor clinical criteria OR presence of 3 minor
clinical criteria
Rejected Infective Endocarditis
OR
therapy OR
No pathologic evidence of infective endocarditis is found at surgery or
Preoperative considerations
Patients should ideally receive 6weeks of antibiotic therapy prior to surgery
(de-creases risk for prosthetic valve endocarditis)
Antibiotics decrease incidence of embolization
Increasing in vegetation size while on antibiotic therapy may predict later
emboli-zation.
Patients with aortic valve endocarditis have a greater chance of heart block
due to the involvement of the conduction system by periannular infection.
Therefore, a preoperative placement of a transvenous pacing wire may be
necessary.
Indications for Surgery
Native Valve Endocarditis
Class I indications:
Surgery should not be delayed if the patient is in cardiogenic shock
LVEDP, elevated LA pressures, or moderate to severe pulmonary
hypertension
Evidence of local extension resulting in aortic or annular abscess, or
from aortic valve endocarditis)
Organisms unlikely to be adequately treated with antibiotic therapy
alone, especially fungal endocarditis.
Persistent sepsis or bacteremia despite antibiotic treatment for at
least 1 week, especially with staph infections. However, it should be
noted that sur-gery during septic shock have a poor prognosis, with an
operative mortality rate exceeding 50%.
Class II indications
Recurrent embolization and persistent vegetation despite antibiotic
treat-ment.
Class IIb indications
Mobile vegetations >10mm in diameter, even if embolization is absent.
These vegetations, especially on the mitral valve, have a greater risk of
emboliza-tion.
Indications for surgery in prosthetic valve endocarditis
Class I
Heart failure, valve dehiscence (unstable prosthesis or perivalvular leak),
evi-dence of increasing valvular obstruction or worsening regurgitation,
abscess formation or heart block, or fungal etiology.
Class II
Persistent bacteremia or recurrent emboli despite antibiotics, or
relapsing in-fection.
Surgical Procedures
Removal of all infected valve tissue, drainage and debridement of abscess
cavities.
Aortic valve replacement, mitral valve replacement.
Tricuspid valve repair is recommended for tricuspid endocarditis, and should
be aggressively attempted especially in IV drug abusers who are more prone
to rein-fection if a valve replacement is performed.
Post op considerations
If intra-operative cultures are positive, 6 weeks of post-operative antibiotic
treat-ment is recommended.
Reference:
Bojar, Robert, M., (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
MYOCARDIAL BRIDGE
Pathology:
Myocardial muscle bride overlying coronary artery. Most are clinically
Severe bridging of the major coronary arteries can produce myocardial
ischemia/infarction, coronary thrombosis, and pre dispose the patient to
atherosclerosis or sudden cardiac death.
As the muscle bridge contracts, it can cause hypo perfusion of the underlying
myocardium due to a buckling in the artery giving the patients angina
30 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 31
Clinical Manifestations:
The most typical symptoms are chest pain, dyspnea, and dizziness, but can
be any typical or atypical angina.
Physical Exam:
Diagnostic studies: Most commonly diagnosed by cardiac catherization.
Cardiac cath: compression of a segment of coronary artery during systole
resulting in narrowing that reverses during diastole
EKG: usually normal
Echo: demonstrates septal buckling and apical sparing
CT angiogram:
Angiogram with FFR and Ivus: to document and further map the length and
Example 1: Bridge during diastole Example 2: Bridge during systole
Management:
Prior to surgery, patients should be trialed on beta blockers and/or non
dihydropyridine calcium channel blockers (ie. diltiazem, verapamil)
Nitrates may exacerbate symptoms and are contraindicated
Indications for surgery
Surgical therapy for those with persistent symptoms in whom ischemic
changes are proven, and for those with a high risk marker (such as life
threatening ventricular arrhythmias, myocardial infarction)
Trial of medical therapy has failed
Surgical procedure:
Myocardial bridge (supra-arterial myotomy): The muscle bridge
is divided directly over the coronary artery. The surgery can be done either
stand-by.
Post-operative management:
Pain control:
Pre-operative placement of paravertebral nerve blocks.
Placed day prior to surgery as outpatient procedure by pain service.
Post operatively patient will receive continuous infusion of
bupivacaine + q6 hour boluses.
Avoid OnQ pump or lidocaine infusion for patients with paravertebral
block
Paravertebral block discontinued day before discharge to ensure
adequate pain control with oral medications
Otherwise, standard post cardiac surgery management
References
Sorajja, P., Iskandrian, A.E. (2016). Myocardial bridge of the coronary arteries. Up to date.
CONSTRICTIVE PERICARDITIS
Constrictive pericarditis results from scarring of the pericardial sac leading to
Etiology/Pathophysiology
Idiopathic or viral
Post-cardiac surgery
Post-radiation therapy
Connective tissue disorder
Post-infectious (tuberculous or purulent pericarditis)
Miscellaneous causes (malignancy, trauma, drug-induced, asbestosis,
sarcoidosis, uremic pericarditis)
Clinical manifestations
Symptoms related to low cardiac output: dyspnea on exertion, fatigue
Physical Exam
Elevated JVP
Pulsus paradoxus, Kussmaul’s sign, pericardial knock, pericardial friction rub,
edema, ascites, and/or cachexia
Diagnosis
Echocardiogram/CTscan gold standard
Operative Procedures: Pericardiectomy
As much of the thickened pericardium is removed as possible
(“pericardial stripping”)
Prior radiation is associated with poorer post-operative outcomes
Post-op Management
surfaces
May have low cardiac output and require inotropic support due to:
myocardial contractile dysfunction
longstanding, irreversible ventricular remodeling
present prior to surgery
References
Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
32 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 33
ADVANCED HEART FAILURE:
VENTRICULAR ASSIST DEVICE (VAD)
Le Ventricular Assist Device (LVAD)
Provides cardiac support and o loading of the LV for patients with
advanced heart failure (acute or chronic). Can be used for bridge to
recovery, bridge-to-transplant or destination therapy
These two are the most common LVADs implanted. Most VAD systems contain
driveline/percutaneous lead, external controller and external battery/power
source
Thoratec HeartMate 2 (HM2) HeartWare Ventricular Assist Device
(HW, HVAD)
of LV to Axial pump. Blood is then
propelled to ascending aorta
Flow: 3 to 10 L/min
Speed: 6000 -15000 RPM, 200 RPM
adjustment interval
Flow estimation is by pump speed
and power
Pulsatility index (PI): the magnitude
pump relating to degree of
contractility during cardiac cycle
over intervals of 15 seconds
Insertion: Median sternotomy; new
approach such as combination
thoracotomy
assist-device/
Centrifugal Pump directly sits at
apex of LV and pumps blood to
Small, no abdominal pocket
needed
Flow: 2 to 10 L/min
Speed: 1800-4000 RPM, 20 RPM
adjustment interval
Flow estimation is by speed, power
and blood viscosity
(delta)
Insertion: Median sternotomy; new
or bilateral thoracotomy
https://www.heartware.com/
products-technology
VAD Parameters:
Speed (optimal)
Produces normal CI
Allows for normal LV size
Allows for intermittent opening of aortic valve (mitigates against stasis of
blood in LV)
Power
Measured in watts
Important to monitor trends (rising watts worrisome for thrombus)
Flow
Calculated, not measured (derived from motor power and speed)
Pulsatility Index (HM2)/
Pulsatility on ow wave
(HW)
Determined by pump speed and the degree of native LV contractility
Pump speed determines the amount of LV unloading (increased speed,
increased unloading)
As speed increases the PI/pulsatility decreases, as speed decreases the PI/
pulsatility increases
Increased preload = increased PI/pulsatility
Decreased preload = decreased PI/pulsatility
Post-op Care Considerations:
Main tenants of post-operative care:
Adjust speed for optimal output (liters per min) and optimal bi-ventricular
shape, interatrial/interventricular septal alignment
Monitor and trend PI (HM2) or Flow pulsatility (HW)
Monitor and trend power
Right Heart Failure
Elevated CVP, decreased step-up or PAPI
Elevated Lactate, Cr, LFTs and other end-organ enzymes
monitor urine output
TTE or TEE
consider more inotrope, iNO, Flolan; IABP and/or RVAD implantation, consult
with Cardiac Surgery
Hypovolemia
Ensure adequate pre-load
monitor urine output
if suctioning, may turn down VAD speed temporarily, consult with ICU
Attending/Cardiac Surgery
administer volume PRN: may need to slow down bolus rate to protect RV
from overload
Blood Pressure
Treat with clevidipine, milrinone, NTG or SNP
However, need to maintain MAP>60 (even >70) for RV and end-organ
perfusion
34 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 35
Bleeding
Check cannulation, invasive procedural sites
May need to delay or pause anticoagulation, consult with Cardiac Surgery
PRN blood products transfusion
consult with Cardiac Surgery before giving any procoagulant
Anticoagulation (when bleeding stops)
ASA 81mg daily for HM2, ASA 325mg daily for HW
Heparin infusion; if HIT positive, consider Argatroban infusion
Titrate to PTT goal (usually starts at 40-60, then 60-80), refer to Cardiac
Surgery Team
Transition to warfarin when stable, adjust for INR goal (usually 2-3)
Be cautious if invasive procedures are needed
Thrombosis
If thrombus present pre-pump
If thrombus present intra- or post-pump: power spikes, increased power and
May need to increase PTT or INR goal
Consider integrelin infusion, tPA thrombolysis or VAD exchange, consult with
Cardiac Surgery
Hemolysis
Monitor CBC (with blood smear), coagulation panel, LDH, haptoglobin, free
plasma hemoglobin
Check LFTs, renal panel, CK
May need to increase PTT or INR goal
Surgery
References
Bojar, R. (2011). Manual of Perioperative Care in Adult Cardiac Surgery.
HEART TRANSPLANT
General Care Guidelines:
I. Hemodynamic Parameters
Tachycardia is normal and preferred
Generally MAPs>65 and up to 100 (if not bleeding) are acceptable
II. Inotropes
Almost all patients will arrive on Epinephrine and Dopamine
Inotropes are not to be weaned w/out discussion with transplant surgeons
Clevidipine rather than weaning inotropes
III. Immunosuppression
A. Induction Agents: to be managed primarily by transplant cardiology team
RATG 1mg/kg on POD# 1, 2, 3
Requires premedication with hydrocortisone, diphenhydramine, and
acetaminophen
Methylprednisolone
500mg IV in OR followed by 125mg q8 x 3
B. Maintenance Immunosuppression
Tacrolimus (Prograf)
Started on POD #1
Goal 12-hour trough 10-15
goal trough and dosing adjusted for renal dysfunction
Started on POD #0
IV and PO doses equivalent
May be held for leukopenia
Prednisone
Started once induction methylprednisolone completed
IV. Opportunistic Infection Prophylaxis
CMV: dependent on Donor vs. Recipient CMV status
CMV IGG
ganciclovir/valganciclovir
Acyclovir
Aspergillus
Inhaled amphotericin
Itraconazole
PCP
Bactrim
Atovaquone if sulfa allergy
Post-operative Care: Critical Concepts
I. Right Heart Dysfunction/Failure
A. Etiology
Pre-Existing pulmonary hypertension
Sub-optimal preservation during procurement (prolonged ischemic time)
Coronary spasm
Air down the coronary arteries
B. Clinical Manifestations
CVP >15 or rising CVP
Hypotension
CVP tracing suspicious of TR
Signs of end organ hypoperfusion
Low UOP
Rising creatinine and LFTs
Rising lactate
C. Diagnositc Studies
TTE
Tricuspid regurgitation
Elevated RVSP
Assessment of bi-ventricular function
Septum bowing towards LV
D. Treatment
Management of patient’s volume status
Aggressive diuresis
Lasix or Bumex gtt
36 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 37
Diuril in addition to loop diuretic
Nesiritide infusion
Consider early initiation of CVVH if inadequate response to diuretics
Escalation of inotropic support
Consider increasing HR (Isuprel vs. pacing)
Restart or increase epinephrine
Consider milrinone
Hypotensive or vasodilated patient may not be able to tolerate
Use cautiously in patients with renal failure
Pulmonary vasodilatation
Inhaled Nitric Oxide/Flolan
II. Bradycardia
Transplanted heart is denervated therefore the resting heart rate should be
higher
Faster heart rate allows less time in diastole thereby protecting the R heart
from over-distention
Monitor HR as inotropes are being weaned. Bradycardia may not become
evident until then.
A. Etiology
Mechanical injury to the conduction system of the heart
Suture line edema
Rejection
B. Treatment
Isuproterinol
Oral theophylline +/- albuterol
Epicardial pacing if available
III. Rejection
Rare in the early post-transplant phase due to induction immunosuppression and
crossmatching of the donor and recipient
A. Clinical Manifestations
Hypotension, poor cardiac output
New S3 or S4
Unexplained heart failure symptoms
B. Diagnostic Studies
TTE
Diminished LVEF
LV thickening
Endomyocardial Biopsy
Normally done weekly beginning 14 days post-transplant
Can be done earlier if high index of suspicion for rejection
IV. Primary Gra Dysfunction
of transplant and is not associated with a diagnosable cause . PGD is a
diagnosis of exclusion.
Unclear etiology, the following may contribute to the development of PGD:
existing donor heart disease, injury to the donor heart during brain death,
organ ischemia during recovery and reimplantation, or re-perfusion injury
Management
High dose inotropy
Addition of IABP
ECMO if the above treatments fail
References
Bojar, R. (2011). Manual of Perioperative Care in Adult Cardiac Surgery.
EXTRACORPOREAL MEMBRANE
OXYGENATION (ECMO)
Veno-Arterial ECMO
Provides cardiopulmonary support (end-organ perfusion, ventilation/
oxygenation and potentially LV depends on cannulation sites) for
patients with severe acute cardiogenic shock.
Peripheral Cannulation Strategies Central Cannulation Strategies
Peripheral cannulated VA ECMO
mostly provides end-organ
perfusion and oxygenation
artery (B)
femoral artery
artery
Central cannulated VA ECMO can
in addition to providing end-organ
perfusion and oxygenation
Potential Complications
Hemorrhage due to systemic anticoagulation
Local Vascular Injury from cannulation
Local bleeding/hematoma
Stroke
PE
Distal Embolization
Infection
Post-op Care Considerations:
General Considerations:
Adjust speed for blood ow/desired cardiac output (liters per min)
Adjust sweep rate for CO2 removal (liters per min)
38 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 39
Keep negative venous drainage pressures (pVein) 0 to -100
Know Pre and Post oxygenator pressures and their trends
“Delta P” = Pre oxygenator pressure – Post oxygenator pressure
Increase Delta P could mean thrombus within oxygenator
Increase in Pre and Post oxygenator pressures may be indicative of
increased resistance distal to oxygenator (thrombus or kink in cannula)
Can control temperature circuit (heat exchanger)
Hypovolemia
Ensure adequate pre-load
Cardiac Surgery
administer volume PRN
HTN
function
Treat with clevedipine, NTG or SNP
Anticoagulation
consider ASA 81mg daily
Heparin infusion; if HIT positive, consider Argatroban infusion
Titrate to PTT or ACT goal (typically ACT goal 140-160), refer to Cardiac
Surgery Team
formation in the circuit
Be cautious if invasive procedures are needed
Inspect for clots in circuit, oxygenator and pump
Bleeding
Check cannulation, invasive procedural sites
May need to pause anticoagulation, consult with Cardiac Surgery
PRN blood products transfusion
Consult with Cardiac Surgery before give any procoagulant
Feiba can be given by the perfusionist post-oxygenator
Hypoxemia
Inspect for clots in oxygenator
Trend Pre and Post oxygenator pressures
Maintain adequate Hgb for O2 carrying capacity
Hemolysis
Monitor CBCs, coagulation panels, LDH, haptoglobin, Free plasma
hemoglobin
Check LFTs, renal panels, CK
May need to increase PTT or ACT goal
Surgery
Veno-Venous ECMO
It only provides pulmonary support (oxygenation) for patients with severe
respiratory failure (ARDS, end-stage lung disease bridge to transplant, acute
lung injury by H1N1 etc). It does NOT contribute to any cardiac output.
Peripheral cannulation strategies:
Internal jugular – femoral vein
Internal jugular only (Dual lumen catheter, Avalon, Protek Duo)
Femoral -femoral (uncommon)
Potential Complications
Hemorrhage due to systemic anticoagulation
Local Vascular Injury
Local bleeding/hematoma
PE
Distal Embolization
Infection
Stroke
Post-op Care/Considerations:
General Considerations
Adjust speed/ow for blood ow (liters per min)
Adjust sweep rate for CO2 removal (liters per min)
Keep negative venous drainage pressures 0 to -100
Patient neck/head position can greatly aect negative venous pressure
and ow
Know Pre and Post oxygenator pressures and their trends
“Delta P” = Pre oxygenator pressure – Post oxygenator pressure
Increase Delta P could mean thrombus within oxygenator
Increase in Pre and Post oxygenator pressures may be indicative of
increased resistance distal to oxygenator (thrombus or kink in cannula)
Can control temperature through circuit (heat exchanger)
Hypoxemia
Inspect for clots in oxygenator
Trend Pre and Post oxygenator pressures
Hypovolemia
Ensure adequate pre-load
40 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 41
Cardiac Surgery
Avalon cannula
Bleeding
Check cannulation, invasive procedural sites
May need to pause anticoagulation, consult with Cardiac Surgery
PRN blood products transfusion
Consult with Cardiac Surgery before giving any procoagulant
Feiba can be administered by perfusionist post-oxygenator
Hemolysis
Monitor CBCs, coagulation panels, LDH, haptoglobin, Free plasma
hemoglobin
Check LFTs, renal panels, CK
May need to increase PTT or ACT goal
Surgery
Anticoagulation
consider ASA 81mg daily
Heparin infusion; if HIT positive, consider Argatroban infusion titrate to PTT
or ACT goal, refer to Cardiac Surgery Team
Be cautious if invasive procedures are needed
Inspect for clots in circuit, oxygenator and pump
References
Cont Education Anesthesia Critical Care & Pain (2012). Oxford University Press
LUNG TRANSPLANT
Fluid and Hemodynamic Management
which are susceptible to pulmonary edema as a result of disruption to the
Monitor indicators of adequate perfusion such as lactate, ScVO2, urine
output, and mental status.
A PA catheter is helpful to guide therapy
If cardiac function is normal, low-dose phenylephrine is preferred since it
Respiratory Management
Ventilator
Set initial tidal volume (VT) at 8-10 mL/kg
Titrate FiO2 to achieve a PaO2 > 80 mmHg. Attempt to wean FiO2 as
much as possible in order to minimize oxygen toxicity and atelectasis.
Keep peak airway and plateau pressures < 30 mmHg. Utilize PEEP for
hypoxia (keep in mind airway anastomosis).
Extremely Important: Monitor native lung hyperination in patient’s
with single lung transplant (e.g. COPD)
Respiratory care post extubation
Encourage frequent coughing and use of incentive spirometer. The
susceptibility to respiratory infection and aspiration.
Start Albuteral and Atrovent for bronchospasms which is common
secondary to reperfusion injury
Pain Control
An epidural is preferred for pain (e.g. thoracotomy or clamshell)
Avoid medications that are sedating or cause respiratory depression
Bleeding
Monitor chest output (Call surgeons/pulmonologist if output > 200 cc/h x 2 h)
Correct coagulopathy
Consider blood products for Hgb < 7, platelet count < 100, INR > 1.5
Keep chest tubes stripped
Immunosuppresion
Induction therapy
Maintenance therapy
Methylprednisone
In OR - Methylprednisolone 500 mg x1 per lung (i.e. for double lung
transplant, administer 1000 mg IV x1)
POD #0 - Methylprednisolone 125 mg IV Q8H x 3
POD #1 - Start Prednisone 0.5mg/kg BID on
Cellcept (mycophenolate mofetil)
Start Tacrolimus 0.5 mg BID (Adjust by 12-hour trough levels) on POD # 1.
Goal trough 12-15-ng/ml
Infection Prophylaxis
Bacterial
Vancomycin1 gm. IV Q12H. Adjust dose to goal trough levels 15-20
Cefepime 1000 mg IV Q8H
PCP (choose one)
Bactrim DS Q MWF (1st choice therapy)
Dapsone 100 mg PO QD
Pentamidine inhaled 300 mg Q month via nebulizer. Need to use with
Mepron (Atovaquone) 1500 mg PO QD
Fungal
Start Itraconazole 100 mg PO BID on POD #2-3
Inhaled Amphotericin B 20 mg BID via nebulizer (as inpatient only). Need
CMV
Donor CMV (-) / Recipient CMV (-)
Acyclovir 200 mg PO BID
Donor CMV (+) / Recipient CMV (-)
Cytogam 150 mg/kg PO. Taper cytogam to 100 mg/kg on POD #14
POD #1 - DHPG / Ganciclovir (if unable to tolerate PO meds) 5 mg/kg
BID
Change to Valcyte if taking orals
42 Disease Processes & Surgical Procedures Disease Processes & Surgical Procedures 43
Valcyte 900 mg PO BID x 14 days then 900 mg QD through 6 months
Donor CMV (+ or -) / Recipient CMV (+)
POD #1 - DHPG / Ganciclovir (if unable to tolerate PO meds) 5 mg/kg BID
Change to Valcyte if taking orals
Valcyte 900 mg PO BID x 14 days then 900 mg QD through 6 months
Oral Candida Albicans (choose one)
Nystatin 5 ml, swish and swallow, TID
Toxoplasmosis
Donor (+) / Recipient (-) and not on Bactrim
Pyrimethamine 25 mg QD for 6 weeks
Folinic Acid 10 mg QD for 6 weeks
Postoperative Complications in Lung Transplant
transplantation.
Risk Factors
Lung injury related to organ procurement, storage, and reperfusion
Donor characteristics include female, African-American race, age > 45
Recipient characteristics include preexisting pulmonary HTN and
Grade severity
Grade 0 - PaO2/FiO2 >300 and normal chest radiograph
Grade 2 - PaO2/FiO2 between 200 and 300
Grade 3 - PaO2/FiO2 <200
Treatment
Treatment is focused on providing supportive care
For hypoxemia, increase FiO2 and PEEP.
Consider increasing sedation to improve ventilator synchrony
Avoid neuromuscular blockade (risk for myopathy)
Inhaled pulmonary vasodilators such as iNO and Flolan are used to
improve ventilation-perfusion mismatch and lower mean pulmonary
artery pressures
Use lung protective ventilation strategies with low tidal volume
Diuresis for goal CVP < 5
Consider extracorporeal membrane oxygenation (ECMO) for patients
with severe PGD who do not respond to maximal conventional
treatment and inhaled pulmonary vasodilators
Acute Rejection
Acute cellular rejection
A1 – Repeat biopsy in 4-6 weeks
Treat based on clinical symptoms
A2-A3
Methylprednisone 10 mg/kg IV daily x 3d
Valvyte 900 mg PO daily x14d
Repeat biopsy in 4-6 weeks
A4
Methylprednisone 10 mg/kg IV daily x3d
Valcyte 900 mg PO daily x14d
Prednisone taper dose 1 mg/kg over 14d then back to baseline dose
Repeat biopsy in 4-6 weeks
Acute antibody mediated rejection (AMR)
Day 1-5
Plasmapheresis daily x5d. One volume exchange with albumin. If
Day 6-7
IVIG 1 gm/kg (IBW) x2d.
Premedicate with Tylenol 650 mg PO and Benadryl 50 mg PO/IV
with each dose
Days 8 & 15
Rituximab 375 mg/sq meter BSA IV weekly x2 weeks
For refractory AMR
Consider the following:
Rituximab and RATG dose.
If patient has worsening AMR, can give 3-5 doses of RATG (1.5mg/
kg/day) QOD.
Bortezomib IV
Photopheresis
References:
Moten et al. (2013). Postoperative Transplant in the Critical Care Unit. American Association of Critical
Care Nurses, 24(4): 345-350.
Lung Transplant Protocol
44 Post-Op Management Post-Op Management 45
POST-OP: NEUROLOGIC: DELIRIUM
Represents an acute change in a patient’s mental status that is associated
with a global impairment in cognitive function
Common, incidence 8-10% overall (up to 20% in elderly patients)
Etiology frequently not clear
may result from microembolization associated with CPB and associated
aortic manipulations
may result from mild cerebral hypo perfusion
Common Contributing Causes:
medication toxicity (including benzodiazepines and analgesics_
metabolic disturbances
Prolonged ICU stay
alcohol withdrawal
low cardiac output syndromes
threshold for cerebral infarction
hypoxia
sepsis
recent/new stroke
Manifestations:
wake cycle
lethargy or agitation
paranoia and hallucinations
Evaluation:
Consider psych consult for severe delirium
review of current medications and drug levels
identify possible history of recent alcoholism or substance abuse
ABG, electrolytes, BUN, creatinine, CBC, Mg, calcium, cultures
Management:
correct metabolic abnormalities
stop inappropriate medications
select appropriate medication to control agitation in the delirious state
Haldol 2.5-5mg PO/IV q6h most commonly prescribed (risk of torsades)
check daily EKG to eval QTC
sometimes makes delirium worse!
Seroquel 12.5-50mg, TID
Precedex drip may be needed while in the ICU. Consider PO version
(Tenex)
Zyprexa 5-10 mg daily
Use melatonin 3-6 mg qhs to help reorient sleep/wake cycle
When in doubt, call psychiatry to aid in management
Benzos may exacerbate acute delirium and should be used only when
managing concurrent alcohol withdrawal
Manage suspected alcohol withdrawal
Benzos usually indicated for several days then should be gradually
tapered
extubation if self-destructive behavior
Also give thiamine 100 mg bid and folic acid 1 mg daily
References:
Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
POST-OP: NEUROLOGIC: PAIN CONTROL
Standing Pain medication orders:
Acetaminophen
Dosing:
650 - 1000 mg, oral/rectal, every 6-8 hours (IV Tylenol should never be used)
Abnormal liver function: 500 mg every 6 hours
Gabapentin
Dosing:
CrCl > 60: 300 mg, oral, three times daily
CrCl > 15 but < 60: 100 mg, oral, three times daily
CrCl < 15 and dialysis: 100 mg, oral, daily
If patient not sedated and having pain, it is reasonable to titrate
gabapentin to 600 mg TID or higher over 2-3 days
Works well in adjunt with Tylenol
discharge
PRN Pain Medication Orders:
(must specify indication mild, moderate, or severe)
Oxycodone 5-15 mg, oral, every 3 hours as needed
Hydromorphone 0.2-0.5 mg, intravenous, every 2 hours as needed
Tramadol 50 mg q6h prn CrCl <30: avoid use
Next step if Tylenol not enough. Usually best for mild to moderate pain
Roxicodone 5-15 mg q4h prn
Next step if Tylenol and tramadol not enough for pain. Usually best for
moderate to severe pain.
drowsiness/delirium
Delirium more prevalent in elderly
Percocet 5/325 mg 1-2 tab PO q4h prn pain
Good for severe pain not relieved with roxicodone
Do not use if patient already on standing Tylenol given risk of Tylenol
overdose
46 Post-Op Management Post-Op Management 47
Dilaudid 2-4 mg PO q4h prn pain, 0.5-1mg IV q3h prn pain, PCA
Used if pain not relieved by roxicodone
Also great for acute pain exacerbations
If require PCA, contact pain service to help manage
Oxycodone 10-20mg PO q12 hours
Consider if not achieving adequate PO pain control with short acting
Roxicodone
Scheduled q12 intervals. Short acting Roxicodone can be taken in
addition for breakthrough pain
Ibuprofen 400 mg, oral, every 6 hours as needed (Needs surgical team approval)
CrCl > 30 but < 60 or age > 65: 200 mg, oral, every 6 hours as needed
CrCl <30: avoid use
Avoid use with dual antiplatelet therapy
Ketorolac 15-30 mg, intravenous, every 6 hours as needed (Needs surgical team
approval)
CrCl <30: avoid use
Avoid use with dual antiplatelet therapy
Only if oral route unavailable; otherwise give oral pain medication
IV pain medication IS NOT the rst line for patients on the oor. Consider increasing
the dose of oral meds for better control. The goal is to prepare the patient for
discharge to home.
Additional medications you may see that you can consider:
Fentanyl 25-50mg IV
Reserve for severe pain not relieved by roxicodone
Commonly given prior to chest tube removal for pain prevention, but the
jury is out on whether this is necessary or not!
Caution with this given heavily sedating
Lidocaine infusion
Commonly started by ICU team
Requires checking daily lidocaine levels
Contraindications:
First and second degree heart block due to risk of worsening heart
block.
numbness and unusual sensations around mouth, metallic taste in
mouth, ringing in the ears, or lightheadedness and dizziness
nausea and vomiting, severe dizziness, decreased hearing, tremors,
changes in blood pressure and pulse.
At serum levels greater than 12 mcg/ml: drowsiness, confusion,
muscle twitching, convulsions, loss of consciousness, cardiac
arrhythmias, cardiac arrest
Ketamine 0.1 mg/kg/hr drip, intravenous, continuous
Consult acute pain service
Local/Regional anesthetic pain modalities
Epidural
Managed by pain service
Commonly used for TAAA
Bupivacaine via On Q pump
See reference page 109
Commonly used for anterior thoracotomy
Paravertebral Nerve Block
Managed by pain service
Commonly used for myocardial bridge
POST-OP: NEUROLOGIC: SEIZURES
A seizure is a “single event characterized by the abnormal excessive synchronized
(Kurle, 2010).
Etiology:
The most common cause of seizures is stroke, 43% within 24 hours of the
stroke
8.9% - hemispheric stroke
8.6% – ischemic stroke
10.6% - hemorrhagic stroke
Intraoperative hypoxia, or air or particulate emboli, metabolic
encephalopathy, cerebral edema
Medications
Lidocaine
Tranexamic acid (a pro-coagulant not used at SHC). Amicar is used at
seizures (though higher rates of renal dysfunction) (Martin, 2011).
Cefazolin (a rare complication), especially in patients with renal
function
Incidence:
0.1% (CABG) to 5% (complex aortic) (Goldstone et al, 2011, Manji et al, 2011,
McGarvey et al, 2013)
59% experience 1 recurrence (Manji, 2011), 89% of those are within 24 hours
Most likely to occur between hours 5-8 postoperatively (Manji, 2012)
Risk factors
Intraop:
Duration of aortic cross-clamp time
Deep hypothermic circulatory arrest
Open chamber surgery
Complex aortic repair (Sharma, 2014, Goldstone, 2011)
Postop:
Metabolic derangements (McGarvey, 2013)
48 Post-Op Management Post-Op Management 49
Considerations
Preoperative Note patients with preexisting seizure disorders and consult Neuro
Critical Care prior to surgery to make a postop plan.
Intraoperative These procedures may decrease the incidence of neurologic
complications (Goldstone et al, 2011):
Epi-aortic scanning before aortic cannulation
Cerebral oxygen saturation monitoring
Retrograde cerebral perfusion with hypothermia or deep
hypothermia during circulatory arrest
Echocardiography-guided de-airing
Postoperative
Review of medications and labs to identify
pro-convulsive agents or toxic serum levels
Generally are isolated events.
Neuro Critical Care team
* The terms simple partial, complex partial, and secondarily generalized are no
longer used
Classication Origin Clinical
manifestations
Guide to
treatment
Focal seizure
(previously
‘partial’)
Origin and spread
limited to one
hemisphere,
arising from the
subcortical or
neocortical regions
Can involve twitching of
a limb, a sense of fear, an
unpleasant smell (aura)
and patients may be
conscious of having them
(Schachter, 2016).
EEG, CT head,
consider Keppra
load and BID
therapy. Lorazepam
if not self-limiting.
Generalized Starts in both
hemispheres
at once, arising
from a cortical
or subcortical
region, may be
asymmetric
Most commonly tonic-
clonic (previously known
as grand mal, with
convulsive jerking in all
limbs), absence (previously
known as petit mal, with
staring or lip smacking,
and myoclonic seizures
(muscle spasms, can be
EEG, CT head,
consider Keppra
load and
BID therapy.
Lorazepam, if not
self-limiting.
Status epilepticus
(SE)
Any type of seizure
can evolve into
“more than 30
minutes of either
continuous seizure
activity or two or
more sequential
seizures without
full recovery of
consciousness
between
(American Epilepsy
Society Guideline,
2016)”.
Characterized as
convulsive or non-
convulsive. This is a
medical emergency.
1st line – lorazepam
or diazepam
2nd line –
fosphenytoin
3rd line –
general anesthesia
* See below for
doses
Treatment
Pharmacologic treatment is not always necessary
seizure, especially if the etiology is obvious and addressed (ie, metabolic
derangement).
Patients with focal neurological decits, epileptiform discharges on
EEG or structural brain lesions are at higher risk for repeat seizures and
should receive anticonvulsive therapy (Kurle & Rutecki, 2010).
Pharmacological treatment:
Loading followed by a maintenance dose of levetiracetam (Keppra) is
Do
Additional antiepileptic pharmacotherapy based on the EEG, CT, and clinical
manifestations of the seizure(s) and response to treatment.
To break a seizure:
1st line: IV lorazepam
depression
2nd line: IV fosphenytoin at 20mg/kg, (can also do VPA 40mg/kg or
Keppra 60mg/kg load – discuss with NCC). Fosphenytoin is better
tolerated over Phenytoin.
3rd line, general anesthesia with propofol or Versed gtts.
Seizures must be dierentiated from myoclonus (4 types)
Physiologic (muscle jerks when falling asleep, causes no disability)
Epileptic (myoclonic jerks in the setting of epilepsy)
Symptomatic (occurring in the setting of a separate neurological disorder)
(Caviness, 2015).
Calling a consult:
Neuro Critical Care Pager number: 14061
Describe the seizure-like activity
Evolution: describe the pattern (ie did it start with gaze deviation and
unilateral shaking which then spread to the opposite side)
Bilateral or convulsive involvement
What were the eyes doing (nystagmus, gaze deviation etc)
Termination: spontaneously or with Ativan
Physical exam ndings
Autonomic changes in absence or focal seizures: tachycardia,
diaphoresis, excess salivation, pupillary dilation, incontinence (Kurle &
Rutecki, 2010).
Tonic-clonic seizures: hypertension, tachycardia, metabolic acidosis,
hypoxia, hypercarbia (Kurle & Rutecki, 2010).
Diagnostic studies:
Head CT without contrast: Perform early to identify potentially reversible
causes (Goldstone, 2011)
Continuous EEG: identify a focal area of seizure activity or the presence of
non-convulsive status epilepticus (Marcuse, 2014)
MRI:
devices (LVAD, ECMO etc), Epicardial wires, certain ICD/PPMs etc.
50 Post-Op Management Post-Op Management 51
POST-OP: NEUROLOGIC: SPINAL CORD ISCHEMIA
Who’s at risk?
branching arteries (Intercostal arteries) providing blood supply to the spinal cord,
potentially resulting in spinal cord hypoperfusion, ischemia and infarction
4. Endovascular repair
a. Incidence: SCI may occur in up to 4% of cases
b.
5. Open repair
a. Incidence: SCI may occur in up to 8% of cases
b.
Intra-op Measures to prevent spinal cord ischemia:
1. Minimize spinal cord ischemic time
2. Increase tolerance to ischemia
a. Deliberate mild systemic hypothermia
b. Ischemic preconditioning (“staged repair”) to allow development of
collateralization of blood supply
3. Augment spinal cord perfusion
a. Deliberate proximal and distal HTN
b. CSF drainage (via lumbar drain placement pre-procedure)
c. Reimplantation of spinal arteries
d. Preserve subclavian artery and hypogastric artery
4. Early detection of spinal cord ischemia
a. Intra-operative neurophysical monitoring (MEP motor evoked potentials,
SSEP somatosensory evoked potentials)
b. Early and serial post-op neuro exam
Post-op ICU Measures to prevent spinal cord ischemia
1. CSF Drainage:
a. Lumbar drain typically placed pre-operatively by anesthesia.
See page 106.
b. Goal to optimize cerebral perfusion pressure (CPP): perfusion to spinal
cord
1. Measured as CPP = Mean Arterial Pressure – ICP
2. We can decrease ICP by removing CSF, thus improving CPP
c. Goal ICP ~10 mmHg (refer to ICU Lumbar drain protocol)
1. Lumbar drain is set open to drain at 10mmHg (14cm H20)
2. When/if ICP is greater than 10mmHg, the lumbar drain will act as a
“pop-o” valve and CSF will drain
d. Must be careful to not OVER DRAIN CSF too rapidly
1. Symptomatic intracranial hypotension:
a. Headache
b. Subdural hematoma
2. Goal: may drain up to 10mL at a time, not to exceed 20mL/hr
2. Augment Mean Arterial Blood Pressure
a. Goal hemodynamic parameters must be discussed with the surgical
attending, as the patient may have residual aneurysm/dissection or
bleeding to take into consideration when establishing goal MAP
b.
used to augment MAP
c. Typical MAP goal 90-100, CPP goal >80
3. Early detection through close neurologic monitoring
a.
b. Q1H Pupillometry while CSF is drained
4. May establish blood transfusion goal for Hct >25 to optimize perfusion
5. Lumbar drain removal
a.
b. POD 2: Clamp x 24 hours
1. Continue to monitor neuro exam, if changes, resume CSF drainage
c. POD 3: Remove if neuro exam intact, monitor for HA or CSF drainage post
removal. Flat for 6 hours post drain removal
If The Exam Changes:
1. Alert ICU attending and surgical team immediately
2. Increase MAP/CPP
a. Increase dose of vasopressors
b. Consider blood/volume transfusion
3. Drain CSF (safely) to decrease ICP and increase CPP
a. Goal ICP <10
b. Drainage not to exceed 20mL/hr
4. Perform thorough neurologic exam
a.
b.
5. Consider consult to neurocritical care
6. Consider advanced imaging (CT/MRI) when stabilized to assess extent of
infarct
References:
References Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
52 Post-Op Management Post-Op Management 53
POST-OP: NEUROLOGIC: STROKE / CVA
Risk Factors:
Pre-Op:
History of previous stroke or TIA (44% of patients with history of stroke
Comorbidities: HTN, DM, Smoking, PVD, Renal dysfunction
Age > 75 (risk of up to 10%)
Carotid disease (Risk is less in unilateral stenosis but as high as 10-15% in
bilateral stenosis > 75%)
Emergent surgery (Type A dissection)
Intra Op:
CBP > 2 hours
High transfusion requirement (especially platelets)
LV thrombus
Air embolization from opening of cardiac chamber
Peri-operative HTN or cardiac arrest
Post op:
Pre-Op & Perioperative prevention:
Avoid hypotension, continue pre-operative ASA, consider need for pre-op
carotid studies
Incidence/Mechanism:
Embolic, most common (~ 2/3 of post op strokes)
Cerebral hyper perfusion
Hemorrhagic
Presentation:
Think BE FAST (Balance, Eyes (vision changes), Face drooping, Arm
weakness, STime — how long since onset of symptoms)
Physical Exam:
Full Neuro exam (CN 2-12)
Strengths of extremities
Pupil exam
“ Blown pupil:” something acutely bad is happening on one side (rising
ICP compresses area that holds one of optic nerves)
“Fixed and dilated” pupils – indicate a prolonged hypoxic injury to the
brain.
Tongue midline
Work-up:
Call Stroke code (dial 211)
CT head without contrast, to rule in/out hemorrhage
MRI/MRA brain with perfusion sequences (Stroke protocol)
Carotid Doppler US study to evaluate for carotid occlusive disease
Medical Management
Blood pressure parameters as determined by consulting teams, but
SBP should not exceed 180mmHg for ischemic and 140-160mmHg for
hemorrhagic cases
Glucose control between 80-140 mg/dL as elevated levels > 200 mg/dL during
neurologic outcome
Avoid hyperthermia
DC all anticoagulation as patient’s condition can worsen, or can be
contraindication for tPA administration
ASA 162mg or 325mg orally or rectally
Antiepileptic therapy as determined by consulting teams
Indications for surgery
General guidelines:
Patients with large hemispheric stroke involving more than two-thirds of MCA
territory (usually only on right-side)
Development of herniation syndrome (i.e. ipsilateral weakness on side of
stroke, lower cranial neuropathies, lethargy)
Uncontrolled intracranial pressure, as dictated by monitor
Surgical Procedures:
Suboccipital craniectomy/craniotomy (for posterior circulation)
Craniotomy/Craniectomy for evacuation of hematoma
Hemicraniectomy
Carotid endarterectomy
Reference:
Winn, H. Richard. Youman’s Neurological Surgery, 6th ed. 2011.
CARDIAC: ATRIAL FIBRILLATION &
ELECTROLYTE REPLACEMENT
Classication of AF:
Paroxysmal (self-terminating) vs Persistent (sustained > 7d) vs Permanent
(typically > 1 year and when cardioversion has failed or is forgone)
Valvular (rheumatic MV disease, prosthetic valve, or valve repair) vs Non
valvular
Lone AF = age < 60 and w/o clinical or echo evidence of cardiac disease
(including HTN)
patients
Management of AF: (see below for treatment algorithm)
For unstable patient, cardiovert immediately if able
If the patient continues to have episodes, consider anticoagulation
(see CHADs score below)
Post-operative Electrolyte Goals:
Potassium (K+) 5.0
Magnesium (Mg+) 2.5
Calcium (CA+) 8.0
54 Post-Op Management Post-Op Management 55
Rate Control for AF: (goal HR 60-80, 90-115 with exertion)
Agent Acute IV Maint (PO) Comments
Metoprolol (BB) 5mg over 2min,
may repeat
q5min x3
25-100mg BID
or TID
↓BP (Rx w/
glucagon).
Watch for CHF &
Bronchospasm
Preferred if CAD
Amiodarone 150mg over 10
min. Then 1mg/
min 6 hours,
0.5mg/min for
18 hours
400mg TID with
taper
Diltiazem (CCB) 0.25mg/kg over
2 min, may
min. 5-15mg/h
infusion
120-360mg/d in
divided doses
gluc). Watch for
CHF. Preferred if
levels
Verapamil (CCB) 5-10mg over 2
min, may repeat
in 30 min
120-360mg/d in
divided doses
gluc). Watch for
CHF. Preferred if
levels
Propranolol (BB) 1mg q2min 80-240mg/d in
divided doses
glucagon).
Watch for CHF &
Bronchospasm
Preferred if CAD
Digoxin 0.25mg q2h up to
1.5mg
0.125- 0.375mg
qday (adjust for
CrCl)
Consider in HR
or Low BP. Poor
exertional HR crtl.
Rhythm Control:
Amiodarone
(Class III)
5-7mg/kg IV
over 30-60min
1mg/min to
achieve 10g load
200-400mg qD
(most eective
drug)
↑QT but TdP
rare. Pulm, liver,
thyroid toxicity.
Check PFTs,
LFTs, TFTs
Sotalol (Class III) n/a 90-160mg BID
Propafenone
(Class IC)
600mg PO x1 150-300mg TID PreRx w/
AVN blocker.
Contraindic. If
structural or
ischemic heart
disease
Procainamide 10-15mg/kg IV
over 1 hr
1-2g bid of slow
release
PreRx w/AVN
blocker
Consider need for Anticoagulation:
Risk of stroke ~ 4.5% per year in non valvular AF. Risk factors include: prior
stroke, TIA, DM, HTN, Older age (>/= 65), HF, CAD, EF < 35%
Who to treat:
Utilize CHAD Score to evaluate patient’s risk and need for anticoagulation
(with no history), consider need for short term (2-3 months post op)
anticoagulation (discuss with attending)
Agent Class Dosing Time to
Peak
Anticoag-
ulation
Half-
life
Renal
Excretion
(%)
Antidote
Warfarin
(Coumadin)
Vit K
Antagonist
0.5-10mg
QD
3-5 days 40
hours
0 Vitamin K
Clopidogrel (Plavix) Platelet
inhibitor
75mg
QD
Prasugrel (Effient) Platelet
inhibitor
5-10mg
QD
7
hours
Dabigatran
(Pradaxa)
Direct
Thrombin
inhibitor
150mg
BID
1-2 hours 14-17
hours
-80 None
Rivaroxaban
(Xarelto)
Factor-Xa
Inhibitor
15-20mg
QD
2.5-4hours 11-13
hours
35 None
Apixaban
(Eliquis)
Factor-Xa
Inhibitor
2.5-5mg
BID
3 hours 8-15
hours
25 None
Endoxaban
(Savaysa)
Factor-Xa
Inhibitor
60mg
QD
1-2 hours 9-12
hours
60 None
CHAD Score (>2 equals indication for anticoagulation)
C
dysfunction)
H Hypertension
A (2) Age >/= 75
D DM
S (2) Prior stroke or TIA or thromboembolism
V Vascular disease (PAD, MI)
A Age 65-74
Sc Sex category female
References:
Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
56 Post-Op Management Post-Op Management 57
CT Surgery Post
Op Atrial
Fibrillation
Treatment
Algorithm
CHRONIC?
NEW ONSET? (will occur in 30-
40% of patients)
-The goal is always first NSR
-If NSR cannot be attained, the
goal then becomes rate control
STABLE?
UNSTABLE?
Amiodarone
150mg/min bolus +
drip @ 1mg/min
OR
Diltiazem 0.25mg/
kg bolus + drip @
5mg/hr (titrate to
heart rate)
DCCV
(direct current
cardioversion)
Successful =
Converts to
Sinus
Unsuccessful
= Remains in
Afib
Continue Amio/
Diltiazem drip until
loaded
Repeat DCCV
Continue Amio/
Diltiazem drip until
loaded
Transition to PO
Amiodarone
starting with
400mg PO TID
Consider Daily
EKG to eval QT
interval.
AF reoccurs?
1. Restart Amio/
Diltiazem bolus +
drip
2. Consider
DCCV
3. Evaluate the
need for
Anticoagulation
Remains in NSR >
24-48 hours
Discharge home
with amio taper
Amiodarone
150mg/min bolus +
drip @ 1mg/min
OR
Diltiazem 0.25mg/
kg bolus + drip @
5mg/hr (titrate to
heart rate)
Afib persists
> 24 hours
Converts to
Sinus
Continue amio drip
@ 1mg/min for 6
hours followed by
0.5mg/min for 18
hours
If HR or BP ↓, first
decrease drip to
0.5mg early. If no
resolution, stop
drip.
S/P MAZE
Goal is RATE
CONTROL
1. Restart Home
meds
2. Restart home
anticoagulation
NSR
Heart rate > 60
Heart rate < 60
Hold home rate
controlling/
antiarrhythmic
medications
Restart home rate
controlling/
antiarrhythmic
medications
(Amio, Sotolol, etc)
NO MAZE
Atrial fibrillation
(will occur in 30%
of patients)
Restart home
Antiarrhythmic/
anticoagulation
medications
MEDICATION DOSING
Amiodarone bolus = 150mg/min over 10 min (max 6-8 boluses in first
24 hours)
Amiodarone drip = 1mg/min x 6 hours, then decrease to 0.5mg/min
x 18 hours (this will load the patient with 1g in the first 24 hours)
If patient becomes hypotensive (occurs in 25% of patients) decrease
the drip to 0.5mg/min early.
After 24 hours on the drip, transition to 400-1200mg PO per day in 2-
3 divided doses. Continue
this loading dose until you have reached
10g total (between IV and PO). Then decrease to maintenance dose
of 200-400mg/day
If QTC interval > 500ms, decrease or discontinue Amiodarone.
Hypotension is more likely to occur in daily doses of Amiodarone >
2g/day. Amiodarone drip should be stopped if 2
nd
degree heart
block or higher occurs or if long pauses are present.
Loading dose of Amiodarone = 10g
D
iltiazem bolus = 0.25mg/kg over 2 min
Diltiazem drip = 5mg/hour and titrate based on heart rate
Due to strong negative inotropic effect, IV Beta blockers should be
avoided.
For patients with
chronic atrial
fibrillation who have
undergone MAZE
procedure, 90% will
be in NSR at 1 year
post operatively
Restart home
medications/
anticoagulation
References
Lee, Richard. Atrial fibrillation and flutter
after cardiac surgery. In: UpToDate, Saperia,
SM (Ed.), UpToDate, Waltham, MA, 2016.
Only consider DCCV for post op
MAZE patients if patient is
unstable or rate is very fast
(DCCV will usually not work until
patient is 4 weeks post op)
Continue to
use IV Amio
bolus until
HR < 10
ANTICOAGULATION
1. Depends on attending preferences
2. Should be considered for any patient having paroxysmal atrial
fibrillation with CHAD score > 2
SPECIAL CONSIDERATIONS
Those with a Low EF or mechanical Mitral valve may benefit from
early DCCV even if they are stable.
CARDIAC: HEART BLOCKS
Post-operative transient disturbances of AV nodal conduction are
more common in patients with:
Low EF, HTN
Severe CAD
Long Aortic clamp time
Low intra-op myocardial temperatures
Aortic/mitral/tricuspid valve replacement/repair
Post-operative conduction abnormalities may occur because of:
Myocardial edema
Suturing
Debridement near AV node/His bundle
First Degree AV Block
Prolongation of PR interval
Treatment considerations:
Epicardial DDD pacing
Avoid nodal-blocking agents
Second Degree AV Block: Mobitz Type I (Wenckebach)
Progressive PR prolongation leading to non-conducting P wave with no QRS
complex
Treatment considerations:
Epicardial DDD pacing
Avoid nodal blocking agents
http://www.zuniv.net/physiology/book/chapter11.html
Second Degree AV Block: Mobitz Type II
Constant PR intervals and
intermittent dropped QRS
complexes (no warning!)
system
More likely to progress to
complete heart block
Treatment considerations:
Epicardial DDD pacing
Stop all nodal blocking agents
Consider permanent
pacemaker
Third Degree (Complete) Heart Block:
Failure of AV conduction of any atrial activity (AV disassociation)
Variable rates for P and QRS complexes
Treatment considerations:
Epicardial DDD Pacing
If atria in AF/A.utter must use VVI pacing
Stop all nodal blocking agents
Consider permanent pacemaker
Heart Block Poem
If the R is far from P,
then you have a First Degree
Longer, longer, longer—DROP!
Then you have a Wenckebach
If some P’s don’t go through,
then you have a Mobitz II
If P’s and Q’s don’t agree,
then you have a Third Degree
58 Post-Op Management Post-Op Management 59
AV Junctional Rhythm/Junctional Tachycardia
Occurs when junctional tissue has faster intrinsic rate than the sinus node
“Junctional escape rhythm:” HR < 60bpm
“Junctional tachycardia:” HR 70-130 bpm
Could be associated with decreased cardiac output due to lack of
synchronous atrial and ventricular contractions
Diagnosis: regular rate with no visible P-waves or retrograde P waves
Treatment considerations:
Stop all nodal blocking agents
Chronotropic Beta-1 agonists to stimulate SA node (ie Isuprel, Dopamine,
Epinephrine)
Epicardial atrial or DDD pacing
For more information on Medtronic temporary pacemaker box,
See page 106.
CARDIAC: CHEST PAIN
The most important etiology in the dierential diagnosis is myocardial ischemia.
Fortunately, it is very uncommon in the post op cardiac surgery patient.
Patient Exam:
Can the pain be reproduced by palpitation, positional changes, or deep
inspiration? If so, much less likely to be ischemic in nature. The most
common cause of chest pain following cardiac surgery is musculoskeletal in
nature.
Obtain Ekg:
Compare with pre op and early post op EKGs
If You Suspect True Angina Follow Mona:
Morphine
O2 via Nasal Cannula
Nitroglycerin (0.4 SL or 1” Nitro Paste)
ASA 325mg
Beta Blocker (metoprolol 5mg IV, may repeat in 5 min.
Cardiac Enzymes for 24 hours (q8H x3) --Troponin/Ck-MB, CK
Consider:
Did the patient of angina pre op? If so, is the pain the same as the pain now?
Any pre operative cath to review?
pneumothorax, pneumonia, pulmonary embolism, sternal wound infection,
aortic dissection, GERD
For inpatient cardiac catherization procedures, page the interventional
cardiology fellow on call to arrange.
CARDIAC: PERICARDIAL TAMPONADE
Pathophysiology:
Manifestations / Physical Exam:
Sudden stop in chest tube output
Equilibration diastolic pressures
early diastole)
Diagnostics:
(If you have started 2 inotropes, and given volume, and the patient is
doing badly (CI < 2.0), you must rule out tamponade)
Chest xray (widened mediastinum)
CBC, Coagulation studies
Treatment:
Give volume, start an inotrope, alert surgical team
Assure chest tube patency
If visible clot within chest tube obstructing drainage, discuss with surgical
resident/fellow about using suction catheter to suction out the chest
tube with sterile technique
If patient acutely decompensating, may require re-sternotomy in the
ICU or OR
Delayed tamponade:
usually resolve completely
clinical symptoms as patients enter a low cardiac output state
Gradual increase in creatinine/BUN
Gradual increase in heart rate
Gradual decrease in urine output
Decrease in exercise tolerance
Diagnostics: Echocardiogram gold standard
Treatment: as above if unstable. If stable, consider pericardial window vs
need to re-open chest in operating room
60 Post-Op Management Post-Op Management 61
CARDIAC: RIGHT VENTRICULAR FAILURE
Pathophysiology
The RV is a thin-walled, crescent-shaped structure characterized by low
resistance, high compliance, and low impedence
Ventriculoarterial coupling is a major determinant of RV function
Etiology
1. Preexisting RV dysfunction secondary to severe coronary disease, pulmonary
hypertension, valvular heart disease, and/or RV infarction
2. Postsurgical RV dysfunction secondary to long cardiopulmonary bypass
(CPB) time, suboptimal myocardial protection, and/or coronary embolism
3.
excessive blood transfusions, pulmonary embolism, protamine reaction,
ischemia-reperfusion injury, tension pneumothorax
4. RV pressure overload secondary to intrinsic pulmonary disease, pulmonary
embolism, and/or acute respiratory distress syndrome (ARDS)
Diagnosis
High right atrial pressure (RAP) and pulmonary capillary wedge (PCW)
pressure. Note this is unreliable when LV dysfunction is also present
May consider TTE to assess IVC, tricuspid regurgitation, right ventricle size,
and septal positioning to guide volume status.
Monitor CVP tracing. With worsening TR and RV dilation, will see rising V
wave on CVP tracing.
Calculate step-up (mean PA pressure - CVP pressure)
Goal > 10
Calculate pulmonary artery pulsatility index (PAPi)
Studied to predict RVAD need in LVAD patients
PAPi = (systolic PA pressure - diastolic PA pressure) / CVP
PAPi >2: good RV function
PAPi 1-2: at risk for RV failure
PAPi <1: RV failure
For more information on Advanced hemodynamic monitoring and PA
catheters see page 125.
Management
1. Prevent elevated pulmonary vascular resistance
a. Avoid hypoxemia, hypercapnia, and acidosis which increase PVR
2. Optimize preload
a. Fluid Administration
i. Administer crystalloids/colloids and/or blood products slowly for low
cardiac output as long as CVP is low or within target range
ii. Do not give additional volume if the cardiac output/blood pressure
does not improve since additional volume may lead to worsening RV
function according to Frank-Starling mechanism
b. Fluid removal
i. Initiate diuretics promptly for volume overload and RV dilation/TR.
Start with Lasix bolus of 10-50 mg IV. If no response to bolus, consider
rebolus, starting Lasix infusion, and/or adding Diuril IV.
ii. If no response to Lasix/Diuril, consider switching to Bumex infusion
or starting Nesiritide infusion. (Note Nesiritide causes systemic
with loop diuretics).
iii. If all the above interventions fail, initiate dialysis.
3.
a. Flolan: inhaled epoprostenol
i. Prostacyclin inhibitor that is a pulmonary vasodilator
ii. Starting dose 0.05 mcg/kg/min. When weaning therapy, titrate down
by 0.01 mcg/kg/min as tolerated
be stopped if suspected
b. iNO
i. Selective pulmonary vasodilator only available in aerosol
administration.
ii. Use only if patient not responsive to inhaled Flolan
iii. Starting dose 20 ppm. When weaning therapy, titrate down by 5
c.
i. Phosphodiesterase (PDE) inhibitor that is both a pulmonary and
systemic vasodilator.
ii. Available in oral doses of 5-20 mg TID
4. Optimize cardiac output
a. Dopamine
doses.
ii. Drip rate ranges between 1-5 mcg/kg/min. May transfer out of ICU on
4 mcg/kg/min
b. Epinephrine
kg/min
ii. Drip rate ranges between 0.01-0.2 mcg/kg/min. Drip titrated by 0.01
mcg/kg/min
iii. Important considerations
1. May cause arrthymias at higher doses
2. Closely monitor CVP/CI/lactates when titrating drip rate
c. Milrinone
i. PDE III inhibitor. Provides inotropy and reduces PVR/SVR
ii. Drip rate ranges between 0.1 – 0.5 mcg/kg/min
iii. Important considerations
1. Long half-life of 1.5-2 hours
d. Dobutamine
SVR
ii. Drip rate ranges between 1-20 mcg/kg/min. Half-life 2 minutes
iii. Important considerations
1. Causes mild tachycardia and hypotension
2. Increases myocardial oxygen demand
5. Optimize right heart perfusion pressure
62 Post-Op Management Post-Op Management 63
a.
b. Vasopressin
i. May cause pulmonary vasodilation at low doses
ii. Drip rate ranges between 0.01-0.04 units/min
c. Norepinephrine
ii. Does increase PVR at higher doses
iii. Drip rate ranges between 1-20 mcg/min
d. Phenylephrine
ii. Like Norepinephrine dose increase PVR at high doses
iii. Infusion rates 5-200 mcg/min
6. Monitor adequate end organ perfusion:
a. SvO2 (either from CCO swan or VBG)
b. Lactate
c. UOP/Creatinine
d. LFT’s (R heart failure leads to hepatic congestion)
7.
consider mechanical circulatory support
a. RVAD
b. VA ECMO
CARDIAC: SYSTOLIC ANTERIOR MOTION (SAM)
OF THE MITRAL VALVE
systole. Typically seen in patients with HOCM or mitral valve repair.
Consider in setting of worsening hypotension with increased inotropic
support
intraventricular septum, papillary muscle displacement, and redundant
Clinical pearls:
To prevent SAM, the goal is to slow the heart rate to prolong the LV lling time
Avoid inotropic support, use vasopressors in setting of hypotension
Avoid hypovolemia, cautious use of diuretic therapy
Once stabilized, consider beta blocker therapy for long term treatment
Reference page 24
CARDIAC: VASOPLEGIA
Persistent hypotension despite adequate cardiac output from low systemic
vascular resistance
response. Risk factors include history of use of ACE inhibitors, ARBs, CCBs,
Amiodarone, B-blockers, and Heparin.
Treatment:
PhenylephrineNorepinephrine
needed
Methylene Blue (1-2mg/kg bolus) inhibits NO synthase and is used in
the treatment of refractory hypotension
CARDIAC: HEART FAILURE
post surgery because most
post surgical state. However
there are some principals that can help you manage the patients.
Medications:
Do not hold heart failure medications (beta blockers, ACE inhibitors,
spironolactone) for low blood pressure. Accept a lower blood pressure
for heart failure patients consider giving them even if your systolic blood
pressure is in the 90’s (even in the high 80’s in some cases).
may be harmful in asymptomatic patients with low LVEF and no symptoms of
Beta blockers:
Beta blockers should be used in all patients with a reduced EF to prevent
symptomatic HF, even if they do not have a history of MI.
Consider Coreg instead of Metoprolol for beta blockade: one study
Metoprolol for heart failure with reduced EF
Aerload reduction:
reduction due to kidney dysfunction. The kidneys will appreciate better
problem
patients who cannot tolerated ACEs or ARBs or who are African American
ACE inhibitors should be used in all patients with a reduced EF to prevent
symptomatic HF, even if they do not have a history of MI.
Diuretics: See volume management below
Volume Management:
Don’t over-diurese patients with preserved ejection fraction. They are very
responsive to volume and cardiac output can disproportionately drop with
minimal changes in preload.
Consider Aldactone or Eplerenone for patients that are on a beta blocker and
ace inhibitor without hyperkalemia
Lasix is a threshold drug- titrate daily dose until you see a response (for
example- if no response to 20mg daily, increase40mg daily instead of 20mg
BID). While inpatient, use IV.
20mg lasix IV = 40 PO = 1 Bumex IV= 10 Torsemide PO
Consider Diuril or Metolazone for patients who are diuretic resistant
If hyponatremic, it is likely a hypervolemic issue. Diuresis is the appropriate
response, rather than giving salt tabs
No pre hydration for cardiac catheterization or CT scan
Consults:
Consider consult to heart failure CNS for assistance with complex patients or
if you have questions. They are also a great education resource for patients.
Enter as epic order.
64 Post-Op Management Post-Op Management 65
PULMONARY: PLEURAL EFFUSIONS
Type of
Pleural
Eusion
Denition Presentation: Common
causes
Pleural Fluid
Interpretation
(Lights Criteria)
Diagnosis Treatment
Transudate
capillaries from: hydrostatic
psi/increased pressure
(CHF, etc)
from nutrition, nephrotic
syndrome, cirrhosis)
Usually occurs bilaterally
Small eusion:
likely
asymptomatic
Larger eusion:
dyspnea, cough,
hypoxia
Physical exam:
percussion
absent breath
sounds over
CHF (most
common -
90%)
Cirrhosis
Nephrosis
Protein ≤ 3 gm%
protein/serum
protein<0.5
serum LDH < 0.6
< 2/3 upper limit
normal
CXR PA & Lateral,
lateral decubitus
CT may be indicated
to evaluate etiology of
US-Guided Diagnostic
horacentesis
c.
protein & lactate
hydrogenase
transudates vs.
exudates.
d. b) PH, total &
counts, glucose,
cytology, gram
stain, culture, etc
exudate subtypes (if
indicated)
Correct underlying condition
Common in immediate post op setting,
consider need for diuresis
Therapeutic thoracentesis for severe dyspnea
Exudate
abnormal capillaries leaking
drainage such as cancer).
Exudates imply local pleural
diseases
Exudates – subtypes:
e. Empyema’s: direct
infection of an exudates.
f. Hemothorax: gross blood
in pleural space from
trauma.
g. Chylothorax: thoracic
duct disruption causes
cholesterol complex
accumulation, usually
associated with
lymphoma and thoracic
surgery.
Can occur bilaterally or
Unilaterally
Usually
inammatory
causes:
Bacterial
Pneumonia
Cancer
Trauma
Protein ≥ 3 gm%
protein/serum
protein > 0.5
serum LDH > 0.6
> 2/3 upper limit
normal
Exudates associated with pneumonias =
parapneumonic pleural eusions.
Step 1: treat pneumonia.
antibiotic.
thoracostomy (chest tube) or surgery.
decortication usually)
Exudates associated with malignancy =
malignant pleural eusions (Lung or breast
cancer common)
Treatment options:
Treat the cancer
may help with symptoms (shortness of breath,
dyspnea, etc).
Pleurodesis.
PULMONARY: PNEUMOTHORAX
Presence of air or gas in the pleural cavity (ie, the potential space between the
visceral and parietal pleura of the lung), which can impair oxygenation and/or
ventilation
1. Etiology
a. Entering the pleural space during surgery or with sternal wire placement
b. Ruptured bleb in patient with underlying lung disease
c. Barotrauma from alveolar overdistention during mechanical ventilation
may manifest as pneumothorax, subcutaneous emphysema or
pneumomediastinum
2. Clinical manifestations
a. Hypoxia, dyspnea, tachypnea
b. Airleak on chest tube: may indicate loose connections along the drainage
system or pneumothorax
c. Subcutaneous emphysema: may develop if air exists under positive
pressure where the pleura has been violated.
d. Tension pneumothorax: collapsed lung causing cardiac compression,
output
e.
3. Treatment considerations
a.
assure chest tube is attached to suction, look for kinks in tubing
b.
oxygen and consider placement of chest tube/pigtail
c. If patient asymptomatic and pneumothorax small, appropriate to
observe with serial chest x-rays
References:
Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
PULMONARY: PULMONARY HYPERTENSION
1. Etiology: related to primary pulmonary arterial HTN or secondary to
elevations of pressure in the pulmonary venous and capillary systems
a. Chronic Pulmonary HTN
i. Congenital heart disease, Connective tissue disease (lupus,
rheumatoid arthritis, scleroderma), Medication/toxin induced
ii. Chronic thromboembolic disease
iii. Lung disease:
OSA
2. Result of pulmonary vascular remodeling from chronic hypoxia and
iv. Le Heart Disease:
venous pressure
1. LV systolic or diastolic heart failure
2. Mitral and aortic valve disease
b. Acute Pulmonary HTN
i. Protamine reaction
1. Type 3 protamine reaction may result in severe pulmonary
vasoconstriction, systemic vasodilation and acute right heart
failure
66 Post-Op Management Post-Op Management 67
2. Typically improves within 10 minutes of stopping protamine
ii. Acidosis/Hypoxemia: lead to increased pulmonary vascular
resistance
iii. Tension Pneumothorax
iv. Pulmonary embolism
v. Acute MR (ie papillary muscle rupture)/LV failure leading to high LA
pressure and pulmonary edema
2. Treatment in the acute setting
a. Identify underlying cause/contributing factors
b. Pulmonary Vasodilators
i. Indications: severe pulmonary hypertension (mPAP > 25 mmHg; RAP >
15 mmHg; CI < 2.0 L/min), right ventricular failure, ARDS with persistent
hypoxia (P:F < 200), and post-op lung transplant with reperfusion
ii. Inhaled aerosol results in dilation of the pulmonary vascular bed
thereby reducing pulmonary artery pressure, pulmonary vascular
resistance, and right ventricular aerload. This results in improved
in VQ mismatch and oxygenation.
1. Flolan (epoprosteronol) *Preferred*
a. Available as IV or aerosol administration. IV administration
(rarely used) causes systemic vasodilation
b. Starting dose 0.05 mcg/kg/min. When weaning therapy,
titrate down by 0.01 mcg/kg/min every hour as tolerated
2. iNO
a. Only available in aerosol administration.
b. Starting dose 20 ppm. When weaning therapy, titrate down by
iii. Sildenal: PDE inhibitor prevents degradation of cGMP and reduces
pulmonary vascular tone
a. Starting dose 10-20mg TID
Sussex, UK: Wiley-Blackwell
PULMONARY: ACUTE RESPIRATORY DISTRESS
SYNDROME (ARDS)
1. Pathophysiology
a.
lungs
b.
capillaries
c. Results in non-cardiogenic interstitial edema
d.
e. Hypoxic and ventilator failure
2. Pre-disposing conditions:
a.
however ARDS only occurs in <1% of patients undergoing open heart
surgery
ii. Sepsis
3. Diagnostic Criteria
a. Acute onset
b.
c. PCWP <18, or no clinical evidence of L heart failure, non-cardiogenic
pulmonary edema
d.
i. P/F ratio = PaO2 ÷ FiO
1. Ex: PaO2 90 on FiO2 40% = 90 ÷ 0.4 = 225
ii. P/F < 200 is associated with signicant shunt and indicates ARDS
iii. P/F 200-300 indicates acute lung injury
4. Management
a. Optimize hemodynamics and volume status, diurese when indicated
b. Optimize nutrition
c.
d. Lung Protective Ventilation (LPV) Protocol: Limits ventilator induced
lung injury
i. Purpose: To maximize gas exchange using low tidal volumes (4-6 mL/
kg) and minimizing plateau pressures (< 30 cm H2O) in all patients
with ARDS
iii. Goals: VT 6 mL/kg, pH 7.30 – 7.45, Pplat > 30 cm H2O, EIP
iv. Prescriber must determine ventilator mode (VCV or PCV) and PEEP
(standard or high)
v. Volume Control Ventilation (VCV)
1. Set VT at 8 mL/kg using patient’s predicted body weight (PBW).
Slowly decrease VT by 1 mL/kg until target VT is achieved
2. Set respiratory rate to baseline minute ventilation (do not exceed 35
breaths/min)
3. Add PEEP at 5-7 cm H2O to goal PaO2 > 55 and SaO2 > 88% (see
table below)
4. Adjust VT to achieve target plateau pressure (Pplat)
a. If Pplat > 30 cm H2O, decrease VT by 1 mL/kg until Pplat < 30 or
VT 4 mL/kg
b. If Pplat < 25 and VT < 6 mL/kg, increase VT by 1 mL/kg until Pplat
> 25 or VT 6 mL/kg
c. If Pplat < 30 and vent dysnchrony, may increase VT by 1 mL/kg to
8 mL/kg and/or increase sedation
5. Adjust respiratory rate to achieve target pH
6. If pH < 7.30, increase RR to max 35 breaths/min
7. If pH < 7.15 and RR 35 breaths/min, increase VT by 1 mL/kg to a max
of 8 mL/kg until pH > 7.15
vi. Pressure Control Ventilation (PCV)
1. PCV is similar to above however end-inspiratory pressure (EIP) is
adjusted to achieve goal VT (tidal volume).
2. If EIP < 10 cm H2O and VT > 7 mL/kg, increase EIP in order to
increase to a maximum EIP 35 cm H2O
3. If EIP is decreased to 10 cm H2O > PEEP and VT > 7 mL/kg or if
patient exhibiting increased work of breathing, consider increasing
sedation. If unable to increase sedation, may increase VT by 1 mL/
kg to max VT 8 mL/kg.
4. Once work of breathing decreased, decreased EIP back to target VT
5-7 mL/kg
68 Post-Op Management Post-Op Management 69
vii. PEEP/FiO2 titration
1. Goal SaO2 88-95% or PaO2 55-80%
FiO2 30% 40% 50% 60% 70% 80% 90% 100%
Standard PEEP 5 5-8 8-10 10 10-14 14 14-18 18-20
High PEEP 8-10 10-12 12-14 14-16 16-18 18-20 20-22 22-24
Sources:
UK: Wiley-Blackwell
Marino, P. (2009). The Little ICU Book. Philadelphia, PA: Lippincott Williams & Wilkins
PULMONARY: ATELECTASIS
Atelectasis: collapse or closure of a lung resulting in reduced or absent gas
exchange
1. Etiology:
a. Obstructive: blockage in the proximal airway leads to nonventilated
alveoli that collapse
b. Passive/Compressive:
c. pain (splinting), over-sedation, or prolonged
supine positioning
2. Clinical manifestations
a. Hypoxia, dyspnea
b.
c. Fever, elevated WBC count, PNA
3. Treatment considerations
a. Identify and address underlying causes:
i. Achieve adequate pain control, decrease sedation
iii. Assess for evidence of PNA and treat appropriately
b. Alveolar Recruitment Maneuvers:
i. Using increased PEEP via ventilator or CPAP
1. Increase mean airway pressure to open closed alveoli to increase
surface area for gas exchange
2. Decrease VQ mismatch/intrapulmonary shunting (improves
ventilation to perfused areas)
ii. Incentive spirometer. Goal volume >1L.
1. Maintains Functional Reserve Capacity (FRC)
2. Prevents and improves atelectasis
c. Bronchial Hygiene Therapy (“Pulmonary Toilet”)
1. Purpose: To help loosen and mobilize pulmonary secretions
2. Indications: mobilization of retained secretions, atelectasis, optimize
delivery of bronchodilators
3. Contraindications: hemodynamic instability, recent facial/oral/cranial
active hemoptysis, nausea/vomiting, radiographic evidence of bled/
bullae, fractured ribs or unstable chest, untreated pneumothorax, and
compromised cardiac status or arrhythmias.
4. Therapies (may be combined with bronchodilating nebulizers for
Acapella Intrapulmonary Percussive
Ventilation (IPV)
Chest Physiotherapy (CPT)
A resistive/vibratory device
that is used to open the
airways and provide
oscillating vibrations to help
loosen secretions
Pneumatic device that
delivers pressurized
minibursts of gas at rates of
100-225 cycles per minute
through a mouthpiece to
achieve alveolar recruitment
Technique that uses manual
or mechanical external
percussion and vibration
to loosen secretions and
promote clearance
Sources:
UK: Wiley-Blackwell
Adams, G. (2006). On Call Surgery, 3rd Edition. Philadelphia, PA: Saunders Elsevier
Marino, P. (2009). The Little ICU Book. Philadelphia, PA: Lippincott Williams & Wilkins
GI: ACUTE HEPATIC DYSFUNCTION
About 25% of patients will develop transient hyperbilirubinemia aer open heart
surgery, but fewer than 1% of patients will have signicant hepatocellular damage
leading to chronic hepatitis or liver failure
1. Risk Factors
a. Preexisting liver disease:
i. Elevated liver enzymes (AST/ALT), elevated bilirubin, or evidence of
synthetic dysfunction (low albumin, high INR)
ii. Elevated bilirubin in patient w/hx CHF is strongest predictor of post-op
liver dysfunction
b. Comorbidities: CHF (high right sided pressure leading to congestive
hepatomegaly), DM, HTN
c. Preoperative cardiogenic shock: may have evidence of “shock liver” prior
to surgery
d. Operative risk factors:
i. Long cardiopulmonary bypass time
ii. Complex operations (ie combined CABG-valve, multiple valves)
iii. Multiple blood transfusions
e. Post-operative risk factors
i. Low cardiac output syndrome
ii. Use of multiple inotropes/IABP
II. Etiology: may result from either decreased liver perfusion or systemic
congestion
Hepatocellular Necrosis Hyperbilirubinemia
Low cardiac output states (requiring
inotropes/vasopressors)
decreased
hepatic perfusion
Right heart failure/severe TR
chronic passive hepatic congestion
Medications (Tylenol, Plavix, statins)
Post-transfusion hepatitis/CMV (late
manifestation)
Hemolysis (paravalvular leak, long
pump run, sepsis, multiple transfusions,
ECMO, drugs)
Intrahepatic cholestasis (hepatitis,
hepatocellular necrosis, TPN, bacterial
infections, medications, benign
cholestasis)
Extrahepatic congestion (biliary tract
obstruction)
70 Post-Op Management Post-Op Management 71
2. Clinical manifestations
a. Jaundice
b. Coagulopathy
c. Refractory acidosis
d. Hypoglycemia
e. Renal failure (hepatorenal syndrome)
f. Encephalopathy
3. Work-up: in addition to basic labs/LFT’s consider further investigation with the
following
a. Order Total and Fractionated bilirubin:
i. Mostly Conjugated (Direct): biliary obstruction (stone, mass, PSC) or
cholestasis (sepsis/hypoperfusion states, cholestasis, TPN)
ii. Mostly Unconjugated (Indirect): hemolysis, hepatic congestion/
decreased bili uptake (heart failure)
b. Assess for hemolysis: LDH, haptoglobin, plasma free hemoblogin,
reticulocyte count
c. Assess for right heart failure/
TR: echo
d. Assess for biliary obstruction/cholecystitis: Alk Phos, right upper
i. Acute Cholecystitis: gall bladder wall thickening, stranding,
ii. Stone/obstruction: stone, ductal dilitation
e. Review medications for hepatotoxicity
f. Assess for acute hepatitis: hepatitis panel
g. Assess for synthetic dysfunction: coag panel, albumin, glucose, lactate
h. Assess for encephalopathy: exam, ammonia level
4. Management: elevated bilirubin usually benign and self-limited post-operative
occurrence. Will gradually improve with normal hemodynamics unless severe
underlying liver pathology is present
a. Address underlying cause
i. Right heart failure/TR: Refer to “Right Heart Failure” section
ii. Bilary obstruction, consider:
1. ERCP/MRCP: for stone in common bile duct w/acute cholangitis (GI
medicine consult)
2. Percutaneous cholecystostomy tube (placed by IR)
3. Cholecystectomy (General surgery consult)
b. Monitor and treat hypoglycemia
c. Judicious reversal of coagulopathy if present
d. Avoid hepatotoxic medications
e. If Ammonia elevated and evidence of encephalopathy: consider
Lactulose 30 Q8
f. Monitor for lactic acidosis (impaired lactate metabolism) and correct pH
with sodium bicarb when indicated
Sources:
UK: Wiley-Blackwell
Roy-Chowdhury, N. Diagnostic approach to the adult with jaundice or asymptomatic
hyperbilirubinemia. www.uptodate.com
GI: CONSTIPATION AND ILLEUS
Cardiac Surgery Post-Operative Bowel regimen:
Medication Dose Frequency Onset of Action
Docusate (Colace) 200mg PO BID 24-72 hours
Polyethylene Glycol (Miralax) 17g Packet Daily 1-4 days
Senna (Senokot) 2 tabs PO qHS PRN 6-12 hours
Bisacodyl (Dulcolax) Suppository 10mg Rectal Daily PRN 15-60 minutes
Magnesium hydroxide (MOM) 30mL Oral Q8 hours PRN
Magnesium Citrate 150-300mL Oral Once 30 minutes- 3 hours
Lactulose 20mg TID Up to 24 -48 hours
Stanford BOMB Sterile water for
irrigation 300mL,
magnesium citrate
200mL, Glucerin Bulk
100% 199mL
Once Immediate
*For VAD bowel regimen protocol see reference materials VAD BOWEL REGIMEN
page 138.
Ileus Management:
Management of ileus starts with correction of underlying medical conditions,
such as sepsis, electrolyte abnormalities, particularly hypokalemia,
hyponatremia, and hypomagnesemia.
Consider need for NG or rectal tube for decompression. For severe illeus-
consider consult to general surgery or GI.
Bowel regimen for ileus management can include BID suppository/enema.
DO NOT USE PERISTALTIC AGENTS FOR ILLEUS MANAGEMENT.
For protracted ileus, contrast studies may be required to rule out mechanical
obstruction.
Discontinue and limit the use of medications that produce ileus (eg, opiates,
narcotics), and use (NSAIDs) instead (unless contraindicated).
Advisable to delay oral feeding until ileus resolves clinically. Consider need
Most cases of postoperative ileus resolve with watchful waiting and
supportive treatment.
see page 91.
GI: POST-OPERATIVE GI BLEEDING
1. Upper GIB: may present as hematemesis, bloody NG/OG tube output, or melena
a. Most commonly from:
i. Stress ulcers (peptic, duodenal, gastric)
ii. Esophagogastritis
b.
reperfusion injury and increased gastric acidity from any of the following:
3. Low cardiac output states
72 Post-Op Management Post-Op Management 73
4. Critical illness
c. Risk Factors
i. Pre-operative: older age, history if PUD/GERD
ii. Intra-operative: long duration of CPB, valve operations, re-operations
iii. Post-operative: low CO, prolonged mechanical ventilation (>48 hours),
coagulopathy, anticoagulation, anti-platelet therapy
d. Preventative measures
mucosa that helps maintain mucosal structural and functional
integrity
ii. Acid suppression
1. Indications for stress ulcer prophylaxis
echanical ventilation for
>48 hours
Spinal cord injury
Use of 2 anti-plt agents
(Plavix, ASA, cilostazol,
ticagrelor, dipyridamole)
Coagulopathy (Plt <50, INR
>1.5, or PTT 2x baseline)
Solid organ transplant in
ICU setting
Any 2 of the following:
Sepsis
ICU stay >7 days
Occult bleed lasting >6 days
High dose steroids w/daily dose
>250mg hydrocortisone
>50mg
methylprednisolone
>60mg prednisone
>10mg dexamethasone
Hx GERD/GI ulcers/acid suppressant
therapy
2. Proton pump inhibitors (PPI’s):
H2 blockers in reducing incidence of hemorrhagic gastritis and
ulceration
a. Pantoprazole 40mg IV/PO daily
b. Use is not without risk!
ii. PPI use is independent risk factor for nosocomial PNA
iii. May cause hypomagnasemia
3. H2 Blockers:
a. Famotidine 20mg IV Q12
b. Associated with thrombocytopenia
e. Treatment considerations:
1. Correct coagulopathy when indicated
2. Consider DDAVP for suspected platelet dysfunction if uremia is present
3. Transfuse blood if hemodynamically unstable
ii. Monitor vital signs for shock. Assess volume status
iii. Flush NG/OG tube if present
iv. If bleeding continues, patient is hemodynamically unstable and/or
there is an inappropriate response to blood transfusion consider
GI consult for EGD (esophagogastroduodenoscopy)
vi. Acid suppression (treatment dosing):
1. Pepcid 20mg IV q8
2. Protonix 80mg IV push + continuous infusion 8mg/hr
2. Lower GIB: dark to bright red blood from the rectum. Color of blood is
associated with the length of time in the GI tract
a. Etiologies:
i. Hemorrhoids
ii. Mesenteric ischemia/ischemic colitis
1. Periods of prolonged hypoperfusion from
a. Low cardiac output state
b. Atherosclerotic embolism or mesenteric thrombosis
2. May present as profound ileus, abdominal pain out of proportion
3. May be associated with elevated lactate, GIB, sepsis (bacterial
translocation)
iii. Diverticulosis
iv. Arteriovenous malformations (AVM’s): See LVAD post-operative
considerations
v. Ulceration/tissue breakdown from rectal tube
b. Work up:
i. Examine patient looking for hemorrhoid or tissue breakdown
ii. Consider placing NG/OG tube to assess for presence of upper GIB
iii.
1. Correct coagulopathy when indicated
2. Consider DDAVP for suspected platelet dysfunction if uremia is
present
3. Transfuse blood if hemodynamically unstable
iv. If bleeding continues, patient is hemodynamically unstable and/or
there is an inappropriate response to blood transfusion consider
GI consult for EGD and/or sigmoidoscopy/colonoscopy
1. If these are negative, source may be small bowel
v. KUB/CT scan to assess for evidence of ischemic bowel
1. Pneumotosis (air in the bowel wall), venous gas, bowel wall
thickening
vi. Radionuclide scanning (ie tagged RBC scan) to localize source of bleed
vii. Angiography:
1. May be diagnostic and therapeutic if bleeding can be localized
detection
Sources:
UK: Wiley-Blackwell
Adams, G. (2006). On Call Surgery, 3rd Edition. Philadelphia, PA: Saunders Elsevier
Marino, P. (2009). The Little ICU Book. Philadelphia, PA: Lippincott Williams & Wilkins
GI: MALNUTRITION (TUBE FEEDING/TPN)
Tube Feeding:
Consult with dietician to evaluate adequate oral intake vs need for tube
feeding.
Use IP GEN Tube Feeding order set to place the following orders:
Consult to nutrition
Place KOF (Small bore feeding tube)
If Feeding tube placed via super user RN with Cortrak, no need for KUB
74 Post-Op Management Post-Op Management 75
to evaluate location
If feeding tube is placed without use of Cortrak, obtain KUB to ensure tip
of feeding tube is post pyloric
If feeding tube is unable to be placed post pyloric, consider use of
Reglan to promote motility.
In some cases, trickle tube feeds may be started while the tip
of feeding tube is in the stomach (beware of increased risk of
aspiration)
Tube feeds are typically started @ 20cc/hr and increased by 20 q8 hours
until goal rate is achieved. (Trickle or trophic TF rate 10-20cc/hr)
Obtain daily labs: CMP, Phos, Mag, Pre albumin (3x weekly)
Glucose management via subQ insulin (Glucose checks q6) or insulin drip
TPN= Total parenteral nutrition
Prolonged ileus. Consult with dietician to assess nutrition needs.
Needs central access (TPN is administered via dedicated line), consider need
for PICC line placement.
TPN must be ordered by 1400. Use IP GEN TPN/PPN Adult Protocol order set
to place the following orders
Consult to nutrition
PICC Line placement if needed for adequate access
TPN + Lipids
Obtain daily labs: CMP, Phos, Mag, Triglycerides
Glucose control via insulin placed in TPN mixture or Insulin drip (some
patients may require both)
dysturbances, loss of gut barrier, acalculus cholecystitis, refeeding syndrome,
& hyperosmolality
GU/FEN: ACID BASE DISTURBANCES
The normal buering systems of the body (bicarbonate, hemoglobin, phosphate,
and protein) are frequently overwhelmed by disease states or altered from the
eects of cardiopulmonary bypass.
reference see page 124.
Metabolic Acidosis:
accumulation of acids in the serum.
1. Anion Gap = Na – (Cl + HCO3). Normal AG 8-12 mmol/L.
a. Correct for hypoalbuminemia. AG + (2.5 x (4-albumin)).
Elevated AG > 13 mmol/L
High Anion Gap Acidosis Normal Anion Gap Acidosis
Lactic acidosis (see below)
Renal failure (reduced acid
secretion)
Rhabdomyolysis
Medications (ASA, ethylene,
methanol)
Ketoacidosis
Diarrhea (high bicarb loss)
Renal Tubular Acidosis (loss of bicarb
resorption)
Carbonic anhydrase inhibitors (ie Diamox,
increased bicarb secretion by kidneys)
Hyperchloremia (increased HCl acid in
blood)
Blood transfusions (addition of aci
2. Lactic acidosis
a. Type A: Impaired tissue oxygenation and anaerobic metabolism from
circulatory failure
i. ICU, immediate post-op considerations—May be result of:
1. Pre-existing renal dysfunction
2. Long pump runs
3. Intraoperative vasopressor use
4. Inadequate O2 delivery during bypass that contributes to
splanchnic and renal ischemia with acidosis perpetuated by a low
cardiac output syndrome
ii. Several days post-op—May be result of:
1. Mesenteric ischemia
2. Sepsis
3. Acute hepatic dysfunction (decreased lactate utilization)
4. Low cardiac output state, malperfusion
b. Type B: Not associated with tissue hypoxia. Low-dose Epinephrine
acid production.
i. Not commonly seen
ii. Consider when cardiac output is adequate and lactic acidosis seems
out of proportion with tissue perfusion
3. Adverse Eects of Acidosis: typically do not occur until pH is < 7.2
a. Cardiovascular:
i. Decreased contractility and cardiac output, decreased liver and renal
perfusion
iii. Increased Pulmonary Vascular Resistance (may lead to Right heart
failure)
decreased SVR
v. Increased risk of ventricular arrhythmias
b. Respiratory:
i. Decreased respiratory muscle strength
ii. Dyspnea/tachypnea from compensatory mechanism
c. Metabolic:
i. Hyperglycemia (tissue insulin resistance)
ii. Hyperkalemia
d. Neurologic:
i. Inhibition of brain metabolism
ii. Obtundation/coma
4. Treatment of Metabolic Acidosis
a. Identify and treat the underlying cause
i. Assess tissue perfusion and cardiac output: VBG/SvO2, Echo, PA
catheter CO/CI
iii. Assess for mesenteric ischemia: lactate, abdominal exam, KUB/CT
iv. Assess for sepsis: CBC, pro-calcitonin, cultures, fever curve
b. Bicarbonate supplementation
i. Normalizing pH may improve cardiac function, improve
ii. Goal is to raise the pH, not to correct bicarbonate levels
iii. Keep in mind that IV Sodium bicarb may result in:
1. Hypernatremia—monitor serial labs, consider D5W/free water
supplementation
76 Post-Op Management Post-Op Management 77
2. Fluid overload from hyperosmolarity—monitor CVP/exam, diurese
when appropriate
SvO2
4. Increased CO2 production from metabolism of bicarbonate
a. May result in respiratory acidosis if patient not adequately
ventilated
b. Monitor ABG, increase respiratory rate on ventilator if able
Respiratory Acidosis
1. Common etiologies: accumulation of CO2 in blood due to hypoventilation
a. Medications: narcotics, benzodiazepines, residual anesthesia, paralytics
b. Stroke/intracranial bleed
c. Acute airway obstruction: sleep apnea, aspiration
d. Hx parenchymal lung disease (O2 delivery may decrease respiratory
drive): COPD
e. Splinting/Limit of inspiration due to pain
f. Pneumothorax
Management:
a. Treat reversible causes: obtain CXR, consider head CT for acutely altered
mental status
b. Consider Narcan for narcotic overdose: Narcan 0.1-0.2 mg q2 minutes
for partial reversal
c. umazenil 0.2mg IV q30
seconds-1min
d. Treat hypoventilation
i. BiPap support ventilation (See Respiratory Care under references)
ii. Consider intubation
Metabolic Alkalosis
1. Common etiologies:
a. Excessive diuresis leading to
i. Potassium loss: directly increases bicarb resorption
ii. Depletion of H+ ions and Chloride (acid loss)
iii. “Contraction alkalosis” = Hypovolemia: stimulates aldosterone
increased bicarb resorption
b. Acid loss from high NG tube output/emesis
c. Sub-Acute/Chronic respiratory acidosis: renal response to chronic
acidosis (ie increased bicarbonate synthesis) takes 12 hours to become
apparent and is maximum at 3-5 days
d. Excessive bicarbonate administration, or administration of agents
metabolized to bicarb
i. Citrate (in blood products) may result in metabolic alkalosis
ii. Lactate (in LR)
2. Adverse Eects of Alkalosis (pH >7.45)
a.
b.
acidosis)
c.
d.
potential hypoxia
3. Treatment of Acute Metabolic Alkalosis
a.
b. Gastris losses: acid suppressant therapy (H2 blockers or PPI’s)
c. Patients with total body water overload (ie post-operative or CHF)
consider:
i. Diamox (acetazolamide): carbonic anhydrase inhibitor that inhibits
bicarbonate resorption in proximal tubule
1. Weak diuretic when used alone
2. Consider use in conjunction with loop diuretic
ii. K-sparing diuretic (spironolactone/eplerenone)
Respiratory Alkalosis
1. Common Etiologies: decreased CO2 in blood stream due to hypoventilation
a. Hypoxia (increased respiratory drive)
b. Anxiety
c. Pain
d. Fever/infection/sepsis
2. Management: treat underlying cause
Sources:
UK: Wiley-Blackwell
Adams, G. (2006). On Call Surgery, 3rd Edition. Philadelphia, PA: Saunders Elsevier
GU/FEN: KIDNEY DISEASE
Acute Kidney Injury
Denition:
Increase in serum creatinine by 0.3mg/dL or more within 48 hours
or
Increase in serum creatinine to 1.5 times baseline or more within the last 7 days
or
Urine output less than 0.5 mL/kg/h for 6 hours
Cause:
hypotension, hypovolemic, HF, renal artery stenosis, renal vein thrombosis,
Cardiac tamponade
due to
Intra Renal: Problems with the kidney itself, ATN/AIN
Postrenal:
kidney stone, BPH, obstructed urinary catheter etc; a bladder scan or a post
void residual to rule out urinary retention
Diagnosis:
Urinalysis: presence of protein (albumin), hemoglobin, granular casts, or
epithelial cell casts may indicate AKI
Urine sodium:
FENa:
an oliguric patient (not accurate if patient has received recent diuretic
therapy)
FENa, % = (UNA x SCr/ SNA X UCr) x 100
FENa < 1 = pre renal disease
FENa > 2 = ATN
78 Post-Op Management Post-Op Management 79
FEU-rea (used for patient who have received recent diuretic therapy)
FEU-rea, % = ((SCr x Urine Urea) x 100)) / BUN x Urine Creatinine
FEU-rea < 35% = pre renal disease
FEU-rea > 50% = ATN
Oliguria: < 0.3ml/kg per hour or < 500mL/day of urine output
Anuria:
Renal US: evaluate for urinary tract obstruction, renal mass, and kidney size
(diagnosis hydronephrosis)
Treatment:
Focused on removing the cause of the kidney injury/ failure.
Discontinue nephrotoxic medications (NSAIDS, Iodinated contrast,
metformin, some antibiotics such as gentamicin.)
Correct low BP or use inotropic meds to increase heart function to
provide good renal perfusion
Avoid IV contrast if possible while creatinine is still up trending
Correct urinary tract obstruction if present (ie insertion of foley catheter)
Continue to trend creatinine and electrolytes closely (cautious electrolyte
replacement)
Monitor volume status closely to ensure adequate hydration without volume
overload
Diuretics may be used for a limited period to relive signs and symptoms
of volume overload.
Indications for dialysis: (consult renal) A-E-I-O-U!
A: Acidosis (pH < 7.1 in those that cannot tolerate correction with sodium
bicarb)
E: Electrolyte Disturbances (ie. Hyperkalemia when k > 6.5 and refractory
to medical management)
I: Ingestion/Intoxication
O: Overload. (Refractory to diuretics)
U: Uremia (altered mental status, uremic platelets)
Chronic Kidney Disease
Denition:
Stage Description
Stage I With normal of high GFR (GFR > 90mL/min)
Stage II Mild CKD (GFR = 60-89mL/min)
Stage IIIa Moderate CKD (GFR = 45-59mL/min)
Stage IIIb Moderate CKD (GFR = 30-44mL/min)
Stage IV Severe CKD (GFR = 15-29mL/min)
Stage V End Stage CKD (GFR < 15mL/min)
Always document stage 3 ckd or higher in h&p, progress notes, and
discharge summary
Post op management:
Monitor post op creatinine closely. Not uncommon to see rising creatinine
in the initial post op period (Acute on Chronic Kidney Injury) but creatinine
should return to baseline by discharge if managed properly
Ensure adequate blood pressure for renal perfusion
Avoid nephrotoxic agents (NSAIDs, metformin, certain antibiotics)
References:
Okusa, M.D., Palevsky, P.M., & Scheidan, A.M. (2016). Overview of the management of acute kidney injury
(acute renal failure). Up to date.
GU/FEN:SODIUM IMBALANCES
HYPERNATREMIA, serum NA >145
Etiologies:
Tube feeding due to lack of free water
Excessive water loss from diuresis or diarrhea
Salt loading from medications (saline drips, sodium bicarb, albumin)
To treat
Add free water to tube feed formula in divided doses (ie 200mL q6h)
Add D5W infusion
And/or encourage water intake if able to take PO
Determine Rate of Correction
Chronic Hypernatremia: present for >48 hours
Correct Sodium by NO MORE THAN 10-12mEq/day
Rapid correction—at risk for cerebral edema (encephalopathy,
lethargy, seizures)
Acute Hypernatremia: present for < 48 hours
Correct Sodium to normal over 24 hours
Monitor serum sodium frequently and adjust free water intake as necessary
HYPONATREMIA, serum NA <135
[mild 130-135, moderate 120-129, severe <120]
Need to determine type of hyponatremia:
Hypervolemic: Na dilution from excessive total body water
Volume overload, CHF, cirrhosis
Hypovolemic: Na and/or water loss
Diarrhea, thiazide diuretics
Normovolemic hyponatremia
Low salt intake, SIADH: syndrome of inappropriate antidiuretic
hormone (Dx of exclusion)
Low serum sodium in our postop patients usually indicates total body water
overload (hypervolemic hyponatremia)
In our patient population, most of concern when Na <130. Otherwise usually
just monitor
Symptoms help determine need to treat (ie headache, nausea, vomiting,
fatigue, gait disturbances, and confusion)
Aim to correct serum Sodium by 4-6mEq/day, no more than 8mEq/day
Risk of rapid correction: osmotic demyelination
If on IV medications, consider giving them in NS versus the standing D5W –
will need to discuss this with the pharmacy
If euvomic/hypovolemic hyponatremia: also consider giving salt tablets
three times daily with meals.
Also can treat with hypertonic 3% saline. If have to go this route, consult
nephrology.
Monitor serum sodium frequently
80 Post-Op Management Post-Op Management 81
HEMATOLOGY: ACUTE BLOOD LOSS ANEMIA AND
POST-OPERATIVE BLEEDING
Acute blood loss anemia and bleeding are expected aer cardiac surgery
(especially for cases on cardiopulmonary bypass)
Contributing factors to post op bleeding:
Platelets
Hemodilution occurs when the circuit is primed and this alone can reduce
platelets by 30-50% (Bojar, 2011). And the longer a patient is on bypass, the more
mechanical stress of going through the circuit, as well.
Heparinization:
protamine itself can will transiently reduce the platelet count by about 30%.
on board. HIT always becomes a concern in a patient who is thrombocytopenic
and has received heparin. This is an even higher risk in pts who have been on
heparin gtts prior to going into surgery and should be evaluated by testing for
antibodies if the patient is showing signs of both bleeding and clotting. (For more
information on HIT see page *** Section IV > 6 > 3. HIT)
Fibrinolysis:
extent can be evaluated using aPTT, INR and D-Dimer but those are very non-
Incomplete surgical hemostasis: with accompanying chest wall bleeding or
anyone with friable tissues.
Preop medications can also play a role in postop bleeding. Any patient who’s
had ASA in the last 7 days will have circulating platelets that are no longer
fondiparanux within 48hrs prior to surgery may have worse postop bleeding since
neither can be completely reversed with heparin.
Managing a bleeding patient:
Chest Tubes
Milk tubes as needed
Careful assessment of hourly output
Warm patient
Hypothermia causes impaired platelet function and suppression of
coagulation cascade
Active warming may be contraindicated in some patients
Control HTN
SNP, NTG, nicardipine, etc.
Sedation/Pain Control
Continue sedation/analgesia until bleeding slows and patient is stable for
weaning/extubation
Re-Exploration
Consider re-exploration for
>400ml/hr x 1hr
>300ml/hr x 2-3hrs
>200ml/hr x 4 hrs
Always consider Cardiac Tamponade as a dierential diagnosis, especially in the
immediate post-operative period. For more information on pericardial tamponade
see see page 59.
Lab Values to monitor:
PT/INR
Treat elevated INR with FFP
PTT
If elevated PTT in isolation or with slight elevation in INR consider treatment
with Protamine
Platelet Count
CPB can decrease platelet count as well as cause platelet dysfunction
Consider platelet transfusion in bleeding patient with platelet <100k or if
patients were taking ASA , Plavix, or IIB/IIIA inhibitors pre-op or are uremic
Fibrinogen
Promotes platelet aggregation and enhances platelet adhesion to the
endothelium
Consider transfusion of cryo if Fibrinogen <100 in bleeding patient
TEG
For TEG interpretation see page 83.
Blood Products/Transfusion Threshold
PRBCs
Clarify transfusion threshold with surgeon
Consider maintaining Hct ~25 in an actively bleeding patient
Each unit should increase Hct by ~3%
CellSaver
May contain a small amount of heparin but is devoid of clotting factors
Platelets
Each unit should increase platelet count by ~42-60k per 6-pk
FFP
Contains all clotting factors
4 units of FFP will increase clotting factors by~10%
Cryoprecipitate
Medications
Protamine
Given for elevated PTT d/t residual heparin or release of heparin from tissue
stores
25-50mg
Half-life 5min, elimination from blood stream in 20-30min
Excessive use of Protamine may increase ACT, cause platelet dysfunction,
82 Post-Op Management Post-Op Management 83
DDAVP
Increases the levels of certain factors (VIII precursors, von Wildebrand’s,
tissue-type plasminogen activator)
Can cause hypotension and peripheral vasodilatation
Feiba
Factor Eight Inhibitor Bypassing Activity
Developed to treat bleeding in pts with Hemophilia A/B.
mostly when pts are given >200units/kg/day.
Start with a quarter dose, or 250 units, up to a full dose of 1000 units for
severe bleeding.
FEIBA is made from human plasma, so the same risk of transmission of
infectious disease is present as when you are giving blood products.
Novo Seven
Promotes localized hemostasis at site of tissue injury and improves INR
Can cause systemic thrombosis
Imaging
CXR
indicative of clot around the great vessels
Echo
TTE or TEE
Stable acute blood loss anemia
like “Expected acute blood loss anemia”
Cont to monitor H/H daily or every other day. H/H usually returns to patients
Treatment: (once able to tolerate PO medications)
Ferrous Sulfate, Slow FE 140mg PO BID
Vitamin C 500mg PO BID
Consider need for epogen injection for severe anemia
Oral Iron and Vit C are usually continued for 1 month post operatively
HEMATOLOGY: TEG
TEG® Clot phase Normal Values Abnormalities Treatment
R Time Clot initiation
4.6 - 8.8 min
Shortened in hypercoagulable states.
Increased R time
= FFP
K Clot Kinetics
Time taken to achieve a certain level of clot strength
1.2 - 2.4 min
and platelet dysfunction.
Alpha
Angle
Clot Kinetics
takes place ( rate of clot formation)
57.7 - 72.9 deg
thrombocytopenia, and platelet dysfunction.
Decreased Angle
= Cryo
MA Clot Strength
Maximal clot strength achieved via GP IIb/IIIa-
59.3 - 76.5 mm
thrombocytopenia
Decreased MA =
Platelets
G Clot Strength
Maximal clot strength achieved via GP IIb/IIIa-
6.4 - 15.0 k d/
sec
Abnormally high in platelet hypercoagulability.
EPL
(Estimated
Percent of
Lysis)
Clot Lysis
0 - 15 % Fibrinolysis =
Aprotonin or
Transexamic Acid
84 Post-Op Management Post-Op Management 85
HEMATOLOGY: HEPARIN INDUCED
THROMBOCYTOPENIA (HIT)
Epidemiology:
1-5% of adults treated with heparin, and a smaller proportion of those who
are treated with low-molecular weight heparin, will develop heparin-induced
thrombocytopenia (HIT).
HIT is associated with a high risk of venous and arterial thrombosis if heparin
is not withdrawn
Diagnosis:
The initial signal is a drop in
noticed, use the 4 T’s score to calculate the likelihood of HIT.
If post op platelet count is low, continue to observe and wait until at least POD
#3 prior to sending HIT panel
1. Thrombocytopenia
2. Timing
3. Thrombosis
Other causes of thrombocytopenia
4. Other causes of thrombocytopenia:
Clinical Manifestations
Thrombocytopenia, but rarely with bleeding events
Markedly elevated rate of thromboembolic events (venous > arterial [4:1
ratio])
7 days)
Diagnosis
HIT functional assay
To order: User HIT panel to order HIT antibody (anti-platelet factor 4 or PF4)
AND Functional assay
Interpretation:
0-3 points = Low probability
4-5 points = Intermediate
probability
6-8 points = High probability
If the PF4 results are indeterminate (0.4-2.0), the functional assay may be
We typically sent functional assay at the same time as HIT antibody as
the functional assay is a send out lab that requires 48-72 hours for results.
Acute Treatment:
When HIT is suspected, a HIT antibody and functional assay should be sent,
and all heparin should be discontinued immediately.
An alternative anticoagulant should be started, EVEN IF THERE IS NO OTHER
REASON FOR ANTICOAGULATION. We typically use Argatroban.
Obtain bilateral LE ultrasounds to rule out occult DVT, which can dictate a
longer course of anticoagulation (3-6 months if thrombosis present vs < 1
month if no thrombosis present)
Long term treatment
until platelet recovery (usually greater than 100). Early initiation of coumadin
has been shown to exacerbate thrombosis and should be avoided.
be overlapped for 3-5 days. Coumadin should be continued for at least 1
month.
As a general rule, patients with documented HIT should not be exposed to
heparin again.
However, it has been shown that heparin may be used again in patients who
were previously HIT antibody positive if the patient no longer has a positive
HIT ELISA antibody titer and the use of heparin is absolutely necessary (ex
cardiopulmonary bypass)
References:
Cuker A & Clines DB. (2012). How I treat heparin induced thrombocytopenia. Blood. 119: 2209-2218.
HEMATOLOGY: DEEP VEIN THROMBOSIS
Denition:
Condition in which a blood clot (thrombus) forms in a view. The clot can limit
Thrombus most commonly occurs in the deep veins in the legs, thigh, or
pelvis (Deep Vein Thrombosis, or DVT)
Risk Factors:
Obesity, smoking, heart failure, history of previous DVT, immobility, cancer,
some medications (such as: erythropoietin, birth control pills, hormone
replacement therapy)
Undergoing a surgical procedure increases risk of DVT development
Diagnosis:
Classis symptoms include: swelling, pain, warmth, and redness of the
Symptoms are usually asymmetrical. Symmetrical swelling is unlike to
represent DVT
increase risk of developing a DVT (therefore treatment with anticoagulation is
not indicated)
US RADIOLOGY VEIN (UPPER/
LOWER/BILATERAL) EXTERMITIES RULE OUT DVT
86 Post-Op Management Post-Op Management 87
D-dimer may also be elevated in patients with DVT
Prevention & Treatment
The main goal of treatment is to prevent a pulmonary embolism, preventing
DVT from becoming larger, and preventing new blood clots from forming
Primary treatment is anticoagulation for a minimum of 3 months
Low molecular weight heparin (SubQ heparin or lovenox)
Unfractionated heparin (continuous heparin drip)
Direct oral anticoagulation: Rivaroxaban (Xarelto), Dabigatran (Sayaysa),
and Apixaban (Eliquis)
Coumadin with goal INR 2-3
Post op DVT prevention includes
Bilatearl LE SCDs on all patients
SubQ heparin (if no contraindication) on patients while in the ICU.
Continue for high risk patients while on iICU.
See reference material see page 134.
References:
Pai, M, Douketis, J. (2017) Patient education: deep vein thrombosis (DVT) beyond the basics. Up to date.
INFECTIOUS DISEASE: SEPSIS
Sepsis
Include two or more of the following:
Temperature > 38°C or < 36°C
Heart rate > 90 bpm
Respiratory rate > 20 bpm
WBC count > 12,000/mm3 or < 4,000/mm3 or > 10% immature
neutrophils
Clinical signs of organ dysfunction
Neuro: altered LOC, hypo/hyperthermia
Pulmonary: hypoxemia, ARDS
Cardiac: hypotension
Renal: AKI (Cr > 2 mg/dL)
GI: hyperbilirubinemia > 2 mg/dL
Hyperlactatemia
Septic Shock
Severe sepsis with hypotension that does not resolve with adequate volume
resuscitation
Sepsis Screening Tool
Goals of Resuscitation
Goals:
CVP 8-12 mmHg, MAP > 65 mmHg, urine output > 0.5 mL/kg/hr, ScvO2 >
70% or SvO2 > 65%, normal lactate levels
Surviving Sepsis Bundle
Resuscitation
large volumes of crystalloids are required
to maintain MAP > 65
Add Epinephrine if additional agent needed to maintain MAP
Vasopressin can be used in combination with Norepinephrine if unable
to maintain MAP
Consider Dopamine in selected patients with marked LV dysfunction. Not
recommended for renal protection
or CO suboptimal
pressures and MAP.
Diagnosis
Obtain cultures before start of antimicrobial therapy if does not delay
treatment (> 45 min)
Blood cultures (one percutaneous and one from each vascular device in
place > 48 hours)
Other possible sites of infection (CSF, sputum, urine, etc.)
Antimicrobial Therapy
Administer broad spectrum antibiotics within one hour of diagnosis
Empiric combination antimicrobial therapy for neutropenic patients or
highly multidrug-resistant infections
Empiric antifungal therapy for high risk invasive candidiasis
Reassess antibiotics daily for descalation
Limit antimicrobial therapy to 7-10 days *
Limit empiric combination therapy to 3-5 days
Narrow coverage following susceptibility results
Stop antimicrobial therapy if cause of SIRS is uninfectious
Source Control
Radiographic imaging if needed
Remove intravascular devices if potentially infected
Surgical resection of infected tissues
Other Support Modalities
Mechanical ventilation
Glucose control
Renal replacement therapy
Blood product administration
Nutrition
Deep vein thrombus prophylaxis
Stress ulcer prophylaxis
resuscitation and vasopressor therapy. Indicated if random cortisol level
<18 mg/dL in patients with septic shock
88 Post-Op Management Post-Op Management 89
INFECTIOUS DISEASE: CELLULITIS
Microbiology:
Most common pathogens are beta-hemolytic streptococci (groups A, B, C, G,
and F), Staphylococcus aureus, including MRSA and gram-negative aerobic
bacilli
Staphylococcus aureus: Periorbital and orbital cellulitis and IV drug users
Pseudomonas aeruginosa: Diabetics and other immunocompromised
patients
Aeromonas hydrophila and Vibrio vulnicus: Cellulitis caused by waterborne
pathogens
Pasteurella multocida and Capnocytophaga canimorsus: Cellulitis preceded
by bites
Streptococcus iniae: Immunocompromised hosts
Rare causes: Mycobacterium, fungal (mucormycosis, aspergillosis, syphilis)
Diagnosis:
For patients with signs of systemic disease (fever or hypothermia, hear rate
[HR] >100 bpm, or systolic blood pressure [SBP] <90 mm Hg) include blood
cultures, drug susceptibility, CBC, creatinine, bicarbonate, CPK, and CRP
levels
Consider use of CT or MRI if suspicious for deeper infection (osteomyelitis/
mediastinis)
Treatment
Medication (see Stanford Antibiogram).
First Line
Treat 5–15 days or longer, depending on response, and guided by culture when
cellulitis (5) [B]. Empiric therapy should be guided by local resistance patterns.
streptococci and methicillin-susceptible S. aureus)
Oral dicloxacillin, cephalexin, clindamycin, or IV cefazolin, oxacillin, or
nafcillin.
Parenteral therapy if severely ill or unable to tolerate oral therapy
cephalosporin; if penicillin-allergic, use clindamycin or vancomycin.
Necrotizing fasciitis and gas gangrene
Parenteral clindamycin and penicillin.
In patients with recurrent infection underlying predisposing conditions,
previous episode of proven MRSA infection, or systemic toxicity, use agents
with activity against MRSA
Parenteral vancomycin, daptomycin, linezolid or oral trimethoprim-
sulfamethoxazole (TMP/SMX), doxycycline or minocycline, or clindamycin
(3)[C].
Mild early-suspected streptococcal etiology
Penicillin G, 600,000 U, and then IM procaine penicillin at 600,000 U
q8h–12h.
Recurrent streptococcal cellulitis
Penicillin IV 250 mg b.i.d., or if penicillin-allergic, use erythromycin 250
mg b.i.d.
Alert
If community-acquired MRSA is a concern, treatment options (7–14 days)
include trimethoprim/sulfamethoxazole: DS (160 mg TMP and 800 mg of SMX)
1–2 PO b.i.d. daily; doxycycline: 100 mg PO b.i.d., or clindamycin: 300–600 mg
PO t.i.d.
Second Line
Mild infection:
If Penicillin allergy: Erythromycin 500 mg PO q6h
cellulitis at current estimated MRSA levels.
0.5 mg/kg/d for 5–8 days) if partial response to antibiotics in hemorrhagic or
bullous cellulitis
Ongoing Care
Follow-Up Recommendations
Repeat blood count if patient is toxic. Repeat lumbar puncture in case of
meningitis.
Consider prophylaxis of deep vein thrombosis.
bacterial antigens. Symptomatic improvement usually occurs in 24–48 hours,
but visible improvement may take up to 72 hours.
INFECTIOUS DISEASE: PNEUMONIA
Description
Community-acquired pneumonia (CAP): Lower-respiratory tract infection not
acquired in a hospital, long-term care facility, or during other recent contact with
the health care system
Hospital-acquired pneumonia (HAP): Pneumonia that occurs 48 hours or more
Ventilator-associated pneumonia (VAP): Pneumonia that develops more than
Health care–associated pneumonia (HCAP): Pneumonia that occurs in a
nonhospitalized patient with extensive health care contact, such as:
IV therapy or wound care within the past 30 days
Residing in a nursing home or long-term care facility
Hospitalization in an acute care hospital for 2 or more days within the
past 90 days
Visited a hospital or hemodialysis clinic within the past 30 days (2)
Evaluation
Symptoms: fever, chills, cough, increased sputum, SOB, pleuritic CP. Note
that the presenting symptoms can be subtle – weakness, malaise, AMS
Other studies:
Blood culture – before antibiotic administration
ABG when patient is severely dyspneic or tachypneic
Consider testing for Legionella (culture and urinary assay), Mycoplasma
(cold agglutinins), Pneumoccocus (urine antigen), Chlamydia (acute and
convalescent serology), or respiratory viral panel if clinical course atypical
or enigmatic
90 Post-Op Management Post-Op Management 91
Sputum gram stain and culture: while controversial, it is helpful if
performed before antibiotics; an adequate sample has >25 PMNs and <
10 epithelial cells.
Consider HIV testing if never previously tested or risk factors for HIV
In Immunocompromised patients, consider diagnostic workup for
opportunistic pathogens (PCP, TB, fungi)
microbiologic diagnosis reduces mortality compared to empiric treatment.
Management
Antibiotic regimen depends on severity of illness, potential for resistant
organisms or opportunistic pathogens
Consult hospital antibiogram and antibiotic guidelines. Adjust for renal/
within 4-6 hours of presentation
Pseudomonas risk factors: structural lung disease (bronchiectasis),
corticosteroid therapy (>10 mg of prednisone per day), broad spectrum
antibiotics for > 7 d in the past month, recent hospitalization, malnutrition
Community acquired MRSA risk: immunocompromised, injection drug use,
necrotizing pneumonia
High risk of multi-drug resistant (MDR) pathogens: late-onset HAP or VAP
last 90 days, high frequency of antibiotic resistance in the community,
immunocompromised, or any risk factor for HCAP above.
Medication
Patient Subset Common organisms Example empiric antibiotic therapy
CAP
- Inpatient
- Not in ICU
Typical: Streptococcus
pneumoniae, Haemophilus
inuenzae,
Atypical: Legionella sp.,
Mycoplasma pneumoniae,
Chlamydophila pneumoniae
Doxycycline 100mg PO BID
(if severe penicillin allergy, consider
CAP
- Inpatient
- In ICU
ASSESS risk of
MDR pathogen
(see above)
As above plus drug resistant S.
penumoniae, Staphylococcus
aureus, other gram-negative rods
Azithromycin 500mg PO/IV x 1 then
250mg PO/IV qday
If risk for CAMRSA: ADD Vancomycin
If risk for Pseudomonas, Pipercillin/
tazobactam 4.5 gm IV q 6h replaces
HCAP, HAP, VAP
(any acuity)
Assess risk of
MDR pathogen
(see above)
Staphylococcus aureus,
Pseudomonas aeruginosa,
drug-resistant Streptococcus
pneumoniae, and other resistant
gram-negative rods.
risk factors for MDR pathogens –
empiric therapy should account for
each individual’s risk factors and
level of acuity.
Low Risk of MDR pathogens:
Doxycycline 100mg PO BID AND
Vancomycin and change doxycycline to
azithromycin in ICU patients.
High Risk of MDR pathogens:
Vancomycin AND
Pipercillin/tazobactam 4.5gm IV q6h AND
INFECTIOUS DISEASE:
C. DIFF (CLOSTRIDIUM DIFFICULT)
Causes:
Produces enterotoxin ( toxin A ) and cytotoxic ( toxin B )
Associated with ALL antibiotics and hospitalization itself
Symptoms: a variety of syndromes are possible from asymptomatic infection ->
diarrhea -> pseudomembranous (PMC) -> toxin mega colon -> fulminant colitis.
Flu-like symptoms: Fever, chills, abdominal pain, watery diarrhea.
Fecal incontinence common.
Diagnose:
a false positive sample
Order only for patients who have had several watery stools. Cannot be
retested before 7 days.
48 hours.
Treatment:
d/c antibiotic if possible
place in contact isolation
Mild: Metronidazole ( Flagyl ) IV
Moderate –severe: Vancomycin oral
DO NOT USE ANTI-PERISTALTIC AGENTS FOR C-DIFF.
INFECTIOUS DISEASE:
URINARY TRACT INFECTION
Denitions:
Lower UTI: Urethritis, cystitis
Upper UTI: Pyelonephritis, renal/perinephric abscess
Uncomplicated UTI: Lower UTI in a non-pregnant woman with normal GU
anatomy
Complicated UTI: Anyone else including upper UTI in women, any UTI in men,
pregnant women or women with structural or neurological GU disease.
Etiology/Risk Factors:
Organisms: SEEEKS PP: Serratia, E.Coli (80%), Enterobacter, Entercoccus,
Klebsiella, Staph. Saprophyticus, Proteus, Pseudomonas
Risk Factors: Female (short urethra), sexual intercourse, indwelling
urinary catheters, or recent instrumentation, diaphragm/spermicide use,
92 Post-Op Management Post-Op Management 93
Treatment:
Uncomplicated UTI:
resistance is > 20%
Lower UTI in Pregnant women:
Amoxicillin/Clauvulanate (Augmentin) and Cephalexin are preferred
Complicated lower UTI: Remove catheter/stent if present (high incidence of
Pseudomonas and Candida).
Uncomplicated pyelonephritis: Low grade fever, WBC count only slightly
elevated, no nausea/vomiting.
Augmentin for 14 days.
ENDOCRINE: ACUTE HYPERGLYCEMIA AND
DIABETES MANAGEMENT
1. General Pre op considerations:
a. Always obtain hemoglobin A1c on pre op labwork
b. For outpatients: instruct them to hold oral meds on the same morning
of OR day; if they are on basal insulin, only give 1/3 -1/2 does the night
before or on the same morning of OR.
c.
continue home DM meds( except metformin) & insulin the night before
surgery; hold oral meds and only give 1/2 -1/3 does basal insulin on the
same morning of OR.
2. Hyperglycemia occurs in virtually all CT surgery patients due to:
a. A. Increased extracellular glucose, decreased insulin secretions and
increase peripheral resistance to insulin due to:
o exposure to extracorporeal circulation
o hypothermia
o release of endogenous catecholamines, cortisol, and glucagon
b. Post-op goal blood glucose is < 180 mg/dL
c. For patients with known high HgbA1c pre op or for any patient
whose glucose is diicult to manage, low threshold to consult
Endocrine.
3. Patients will be admitted to the CVICU on an insulin drip. Patient should
remain on an insulin drip until blood glucose remains within target range
with stable drip titrations (+/- no more than 1 for past 4 hours)
a.
b.
NS @ 50mL/hr and d/c D5 ½ NS.
Preparation Onset Peak action Duration
Rapid Acting
Insulin Lispro (Humulog)
Insulin aspart (NovoLog)
9-30 min
15 min
30 min-2.5 hrs
30 min-1 hr
3-4 hrs
1-3 hrs
Short Acting
Regular insulin
30 min- 1 hr 2-5 hrs 3-8 hrs
Intermediate Acting
NPH
1-4 hrs 4-10 hrs 10-16 hrs
Long Acting
Insulin glargine (Lantus)
2-4 hrs None 24 hrs
94 Post-Op Management Post-Op Management 95
c. Special Circumstances
4. Preparing for discharge:
a. For patients with no previous history of diabetes, the goal is to wean
i. If no formal diagnosis of Diabetes, but pre op A1C > 6.4%, consider
consult to endocrine or initiation of oral anti diabetic agents
ii. If a patient is being discharged home with any new diabetic
medications (oral or injection), Diabetes education must be ordered
(~2 days prior to discharge) and completed by with DM Nurse or the
bedside RN
iii. Diabetic teach orders in Epic
1. “Diabetes education” = Bedside Nursing
a. Can also place nursing communication order for RN to initiate
DM Teaching Video
2. Nsg Referral to Diabetes RN = CNS Specialist (*Preferred)
b. For those patients with diabetes, slowly restart any oral anti-diabetic
agents and or insulin. Patients will likely be on much lower doses of
medications or insulin at discharge than at pre op
i. Medications can slowly be up titrated as needed in the outpatient
setting as patients diet and appetite returns to normal
ii. Oral Antidiabetic agents:
1. Metformin
a. Contraindicated in the prescence of renal dysfunction (Creat >
~1.5)
b. Metformin should temporarily be held pre and post
administration of IV contrast
c. Typically held 48 hours prior to any major surgery. Resume
returned to baseline.
2. Sulfonylureas (Glipizide, Glimepiride, Glyburide)
a. Stimulates insulin release from pancreas
b. Glipizide does not have an active metabolite, better choice for
those with renal failure
c. Overall, increased incidence of causing hypoglycemia
3. Thiazolidinediones ( Actos, Avandia)
a. May exacerbate heart failure! Avoid use in most cardiac patients
96 Post-Op Management
ENDOCRINE: ADRENAL INSUFFICIENCY
Denition:
Most commonly occurs in critically ill patients due to subnormal
corticosteroid production.
Diagnosis:
Total (random) serum cortisol: Low
Morning serum cortisol concentration: Low (> 3mch/dL)
CTH Stimulation test:
Administration of ACTH (1-24) or Cosyntropin:
Stanford high dose test (250mcg)
A normal response is a rise in serum cortisol concentration 30-60
A normal response to high dose ACTH stimulation test excludes
Low dose test (1mcg)
A normal response is a rise in serum cortisol concentration 20-30
Treatment: Stress Dose Steroids
Consider treatment when patient on >2 pressors with hemodynamic
instability
Replacement with hydrocortisone:
50mg IV Q6 hours or 100mg IV q8 hours
Consider quick taper (over 3-5 days) once hemodynamics improve
References:
Procedures/Devices 97
PROCEDURES: ATRIAL ELECTROGRAMS
Requires the presceince of atrial temporary epicardial wires
To perform:
Obtain standard ECG for baseline/comparison
For Atrial ECG: Attach the two arm leads to the atrial wires (all other leads
attached normally)
A bipolar ECG will be recorded in Lead I and unipolar ECG in Lead II or III
Interpretation: Evaluate atrial activity in relation to QRS complex
Interpretation examples:
Normal Sinus rhythm: Large atrial spike on Atrial ECG will correlate
with P waves
Junctional: No atrial spike present on Atrial ECG
PROCEDURES:
DIRECT CURRENT CARDIOVERSION (DCCV)
Supplies/Equipment
5.
6.
7. EKG machine
8. Monitoring equipment at bedside (bedside telemetry with 5 lead system,
oxygen access and mask, pulse oximetry, ambubag)
Procedure
Pre-Procedure Care Steps:
1.
a. 12 lead EKG
b. Patent intravenous venous line (IV)
c. Patient is connected to the following: telemetry with a 5-lead EKG
equipment, oxygen is available/operational, ambu bag at bedside
2. Keep patient NPO for approximately 6 hours prior to procedure
3.
4. Obtain written informed consent
5.
98 Procedures/Devices Procedures/Devices 99
For patients on Telemetry unit requiring DCCV: (must be performed by
Cardiac Anesthesia)
1. Page, call, or text ICU Cardiac Anesthesia Attending on call directly to set
up cardioversion
2. Call OR to book the case in the OR (this is for ICU attending billing
purposes)
Cardiac anesthesia on call for the OR should only be contacted for cardioversion
if ICU Attending is unable to perform the procedure.
PROCEDURES: PACER WIRE (PW) REMOVAL
Pre Removal Checklist:
1. Are PW capped with no evidence of rhythm issues on telemetry for 24 hours?
2. If pacing wires have not been capped yet, any pacing activity in last 24 hrs?
(Check with primary nurse and telemetry monitor). If not > cap pacing wires.
3. If PW already capped, for how long? (Usually require wires to be capped for at
least 4-6 hours before removal)
4. Is patient on any anti-coagulation including Heparin sub Q/ IV infusion,
Argatroban, Plavix, Coumadin, Pradaxa, Xarelto, Eliquis etc?
i. In general, we do not start non-reversible anticoagulant agents (Plavix/
Pradaxa/Eliquis/Xarelto, etc.) until PW already removed
ii. If novel OAC agent has been started, check with surgical team regarding
timing of holding medication prior to PW removal
iii. If on SubQ heparin, hold Sub Q heparin 6-8 hrs before PW removal
iv. If on heparin/argatroban gtt, hold gtt for 6 hrs before PW removal, and
v. If on Coumadin, slowly titrate Coumadin dose until PW out, and only
remove PW with INR < 2.0.
5. Was PW sutured in or oversewn to heart? Double check sign-out list and
notes. *** In this case PW are to be CUT AT SKIN, not pulled ***
6. Has plan to remove PW been discussed with attending or chief resident?
During Removal:
Maintain smooth and steady strength
swab
Aer Removal:
Notify both patient & primary RN to keep patient in bed for at least 1 hour
Instruct RN to watch for warning signs and symptoms of tamponade such as:
Lightheadedness
Dizziness
Diaphoresis
Chest discomfort
Decreased BP
Increased HR
6.
i. Anticoagulation:
• If duration of atrial arrhythmia < 48 hours, no anticoagulation required
• If duration of atrial arrhythmia > 48 hours, consider anticoagulation in
conjunction with CHADs score
ii. K+ - consider replacement if K+ < 3.4
7. Review baseline vital signs and SaO2 from pulse oximeter
8.
9. If temporary pacing wires present- ensure attached to external pacemaker
box and turn pacemaker box on (consider placing patient on back up VVI
mode)
10.
placement is at least six (6) inches away from implanted device
11.
i.
attending provider’s discretion)
ii.
iii. Press “Sync” button and ensure R wave aligns with synchronized
marker
iv. Press record button to ensure recording paper is operational
Procedure Steps:
1. Perform “Time out”
2. Anesthesiologist/ICU APP administers anesthetic agent via IV with O2 on
patient
3. Vitals signs and SaO2 are recorded every minute by RN
4. When anesthesiologist/ICU APP determines patient is adequately sedated,
he/she acknowledges to the APP that patient is ready for DCCV
5. The APP performs the following:
i. Press the “Charge” button and states loudly, “Charging”
ii. States loudly, “All clear!” and visually sweeps the bed to ensure no one
is touching the bed and waits for other team members to verify they are
clear
iii. Press and hold the “Shock” button
6.
communicates with anesthesiologist to verify vital signs are stable
7. If patient remains in sinus rhythm, anterior/posterior pads are removed from
from patient
8. If patient has early re-initiation of atrial arrhythmia or remains in an atrial
arrhythmia, DCCV procedure is repeated with a higher number of joules. APP
energy for the maximum of 3 shocks.
9. The APP follows current ACLS protocol for asystole, high degree AV block or
ventricular arrhythmias and pages Attending Physician
10. The APP completes the following:
i. Reviews post procedure EKG
ii. Any medication reconciliation, if applicable
iii. Document via Procedure Note: Include medication administered, # of
joules, # of shocks, post procedure rhythm, and any adverse events.
100 Procedures/Devices Procedures/Devices 101
If the chest tube has purse strings:
1. With scalpel, cut the holding suture which is tied around the chest tube and
the purse strings on the distal end, make sure leave enough purse string
length to tie.
2.
3. Instruct the patient to take deep breath in and hold breath. (*Tubes may be
pulled at end inspiration or end expiration, the important point is that the
patient is not inspiring as the tube comes out)
4. Pull chest tube smoothly and quickly
5.
removal, operator immediately tie down the purse string with surgical knots
X3 and cut excess string with scalpel
6. Remind patient to breath normally as soon as chest tube is removed
7. Cover the CT site vaseline gauze with dry dressing and tape
If the patient does not have purse string to tie:
1. Cut the holding string and cover the insertion site with Vaseline gauze quickly
while removing the chest tube
2. Cover the Vaseline gauze with dry dressing and make sure the whole dressing
is sealed well with 2inch paper tapes for @ least 48 hrs before remove
dressing or shower
If chest tube is pigtail catheter placed per IR
1. See Pigtail removal
Check list post chest tube removal:
Dispose all sharps in sharps container; dispose CT drainage unit into doubled
red trash bag
If concern or suspect post CT removal PTX, need to check CXR immediately; if
no concern for PTX, do not need to check CXR
extreme pain, postop PTX etc.) during or postop procedure
Post chest tube removal patient education:
Keep occlusive dressing or stiches on for at least 48 hrs, then remove and
clean site in shower (CT stich could be removed prior to discharge or on clinic
visit time)
No soaking in bathtub for 1 week
CT insertion site will be assessed at follow up MD visit in 1-2 weeks
increasing erythema on CT sites
Pigtail Removal (placed by IR)
PROCEDURES: RAPID SEQUENCE INDUCTION
Simultaneous administration of a sedative and a neuromuscular blocking
to facilitate emergent endotracheal intubation and to minimize the risk of
aspiration.
Administer:
1) SEDATIVE; 2) PARALYTIC; 3) FLUSH
(Most Common combination is Etomidate and Rocuronium +/- propofol for side
eect prole)
If the patient starts to exhibit s/sx of tamponade
follow these steps:
1. 1. If patient only has symptoms, but BP and HR are stable:
i. Order STAT Echo
ii. Call Echo lab (x54160) to notify them of order and that the purpose is to
rule out tamponade
iii. Continue to monitor patient & vitals closely. Run BP checks Q15 min.
iv. Notify chief resident or attending
v. As soon as there is a change in vital signs, follow step 3.
2. If the patient’s BP starts to drop, but general condition is OK
i.
ii. Order STAT Echo, call Echo lab and notify as above.
iii. Notify chief resident and attending that you have suspicion for
possible tamponade
iv. Call ICU team for possible transfer to back to ICU
3.
decompensating quickly, take all steps as listed above but notify on call
attending and OR that emergent surgery is needed. If patient goes into
cardiac arrest or mental status starts to change, etc
i. Activate Open chest code and rapid transfusion protocol.
ii. Open chest at bedside ASAP to release pressure on heart
•
• Direct CPR/cardiac massage if cardiac arrest
• Straight to OR
Chest Tube Removal:
Things to consider before CT removal:
If drainage < 150 cc/24 hrs (some surgeons are OK with drainage< 200cc/24
Is there any air leak from chest tube?
If chest tube with persistent air leak, may switch to water seal overnight
and check CXR next AM, if no new PTX or previous existing PTX in stable
size-> may remove chest tube (sometimes needs to clamp chest tube 1st
and repeat CXR to rule out new PTX/increasing PTX size before removal)
Is there any PTX on CXR?
Assess pain control need: usually give fentanyl 25-50 mcg IV or dilaudid 0.2mg
IV before procedure
Grab materials to use: suture removal set or scalpel; multiple 4x4 gauzes;
Vaseline gauze; hem clamp; 2 inch wide paper tapes; blue chux ; 2 red
biohazard trash bag
Usually needs a 2nd person (RN or PA/NP colleague to hold chest tube site
tissue together before knots are tied or Vaseline gauze is placed)
Procedure:
Place patient in bed with comfortable position and explain to the patient
about the procedure process
Remove chest tube site dressing and assess the wound
If there are 2-3 tubes connected together with Y-connector, need to clamp
chest tube removal
102 Procedures/Devices Procedures/Devices 103
PROCEDURES: BRONCHOSCOPY
Indications for bronchoscopy:
Hypoxemia
Suspected airway obstruction
New CXR opacity
Copious secretions
To obtain Bronchial Alveolar Lavage (BAL)/sputum culture
Pulmonary toileting
Setting up a bronchoscopy:
Discuss with attending on ideal time and indication
Decide bronchoscope (full cart) vs ambuscope (smaller screen, smaller
scope)
Full cart bronchoscope indicated for:
Thick secretions, copious secretions
Copious bloody secretions
Attending preference
Call x37709 (RT bat phone for charge RT). They will ask the following:
Patient name, location
Attending provider
Indication
Scope required (ambuscope vs bronchoscope)
Aer the bronchoscopy:
Fill out the order requisition:
Pneumonia diagnosis code: 498
Gram stain and culture for BAL
Order post-bronchoscopy CXR
DEVICES: IABP
Indications
Cardiogenic shock
Unstable angina
Intractable ventricular dysrhythmias
Threatening extension of MI
Prophylactic support for PCI
Prophylactic support for OR induction
Post-op myocardial dysfunction
Inability to wean from CPB
RV support during LVAD implantation
Contraindicated in Aortic regurgitation, Aortic dissection, or with severe aortic
of peripheral atherosclerosis
Placement/Position
1-2cm below L subclavian artery and above the renal artery branches
Tip should be between the 2nd & 3rd Intercostal space on CXR
Sedatives
Drug
Name
Class Benets Contra-
indications
Notes Dose
Etomidate Imidazole
derivative
Excellent
sedation
with little
hypotension
Known to
suppress
adrenal cortisol
production
Use cautiously
if patient
has sepsis;
initial dose of
glucocorticoid
may be needed
0.3 mg/kg
Ketamine Phencyclidine
derivative,
dissociative
anesthetic
Stimulates
catecholamine
release
Bronchodilation
Use in patients
with elevated
ICP or elevated
blood pressure is
controversial
May be an
excellent
induction agent
for patients with
bronchospasm,
septic
shock, AND
hemodynamic
compromise
1 to 2 mg/kg
Midazolam Benzo-
diazepines
Potent dose-
related amnesic
properties
Dose-related
myocardial
depression
can result in
hypotension
0.2 to 0.3
mg/kg
Propofol Alkylphenol
derivative
Bronchodilation No absolute
contraindications
Dose-related
hypotension
Paralytics
Drug Name Class Contraindications Notes Dose
Succinylcholine Depolarizing
agent binds to
postsynaptic ACh
receptors causing
continuous
stimulation
Hx or family hx of malignant
hyperthermia
Hyperkalemia or risk of
developing hyperkalemia
Upregulation of ACh
receptors predisposes pts to
hyperkalemia
Neuromuscular disease
involving denervation
(muscular dystrophy, stroke
>72hrs, spinal cord injury
>72hrs, muscular dystrophy,
ALS)
Rhabdomyolysis
Burn > 72 hours old
Inherited myopathies
Crush injuries >72hrs
Severe infection w/ exotoxin
(tetanus, botulism)
Note: Succinylcholine is safe
in myasthenia gravis
paralysis occurs
in 45 to 60
seconds
duration approx.
6- 10 min.
1.5 mg/kg IV
Rocuronium Nondepolarizing
agent.
Competitively
inhibits ACh
receptors
preventing
depolarization
Paralysis occurs
in approximately
45 to 60 seconds
duration approx.
45 minutes
1.0 mg/kg
IBW
Vecuronium Nondepolarizing
agent.
Paralysis occurs
w/in 2.5-3 min
Duration 25-40
min.
0.08-0.1
mg/kg
104 Procedures/Devices Procedures/Devices 105
Possible Reasons for Poor Augmentation
Patient’s native stroke volume > IABP volume
Indication of readiness to wean from IABP
Balloon too small?
Low SVR
Hypovolemia
IABP positioned too low
Kinked catheter
Triggers
Autopilot Mode
Machine selects EKG and AP (arterial pressure) source, trigger mode and
timing method as well as optimizes timing
Machine continuously monitors the patient and chooses the best trigger
mode based on patient condition
EKG
Pre-set trigger mode
EKG Peak
Best for wide complex rhythm
Best for HR>130bpm
A Fib
Best choice for varying R-R intervals
Arterial Pressure
Best trigger when EKG is unavailable or has lots of artifact
Triggered by the systolic up-stoke of the arterial pressure waveform
Should be used during CPR
A Pace
Triggered by the atrial pacing spike
Can only be used if patient 100% A paced
V Pace
Triggered by the ventricular spike
Can be used if patient V paced or AV paced
Pt must be 100% paced
Internal
activity
Used in situation when there is no cardiac output and no EKG
During CPR
Arterial pressure trigger should be selected as this will synchronize counter
pulsation to cardiac compressions
IABP Complications:
Distal limb ischemia (most common complication occurring in 10-15% of
patients) and compartment syndrome
Infection and sepsis
Thrombocytopenia
Balloon rupture, may lead to helium embolus
Risk and complications of insertion:
coverage
If balloon is too low = decreased visceral organ perfusion (decreased
urine output)
Aortic dissection during insertion
Basic Principles
just prior to systole
aortic valve closure
This combination favorable alters the myocardial oxygen supply: demand
ratio (Increased myocardial perfusion with less work)
May be indicated in RV failure:
Improvement in RV perfusion from diastolic augmentation
Improvement in LV function from unloading
Deation phase of IABP leads to
Increased stroke volume
Enhanced forward cardiac output
Ination phase of IABP leads to
Increased diastolic pressure
Potential for increased coronary collateral circulation
Increased systemic perfusion
Timing
Ination
Rapid rise in aortic pressure which increases O2 supply to coronaries
Augmented pressure should be > systolic pressure
Deation
Reduce aortic and end diastolic pressure, improving CO
Assisted end diastolic blood pressure </= unassisted end diastolic blood pressure
Assisted peak systolic pressure should be <unassisted peak systolic pressure
IABP tracing at 1:2 ratio. IABP end diastolic pressure is lower than the patient’s
aortic end diastolic pressure. The balloon assisted peak systolic pressure is lower
than the systolic pressure that is generated without a preceding assisted beat.
106 Procedures/Devices Procedures/Devices 107
placed. The ventricular wire is the shorter one. Occasionally, 2 ventricular
wires are placed (will be equal length) » either one can be used as the ground
lead.
The ventricular wire is inserted into the negative pole of the temporary
external pacemaker. The skin wire is inserted in the positive pole.
Unipolar vs. Bipolar
Unipolar wires consist of a single negative wire attached to the epicardium
and an additional wire in the subcutaneous tissue (positive).
Bipolar system consist of a single wire with two conductors (positive and
negative) which are both attached directly to the epicardium
threshold to obtain capture and is less sensitive to electrical interference
when sensing compared to unipolar system.
General Concepts
Stimulation or Capture Threshold
Refers to the amount of energy delivered by the pulse generator in order to
initiate depolarization (measured in milliamps).
The usual starting point is 10mA and slowly increased until capture is
achieved.
electrodes.
How to determine appropriate output threshold setting:
Set RATE at least 10 ppm above patient’s intrinsic rate.
Decrease OUTPUT: Slowly turn OUTPUT dial counterclockwise until ECG
shows loss of capture.
Increase OUTPUT: Slowly turn OUTPUT dial clockwise until ECG shows
consistent capture.
This value is the stimulation threshold.
Set OUTPUT to a value 1.5-2 times greater than the stimulation Threshold value.
This provides at least a 2:1 safety margin.
Troubleshooting Failure to Capture
Possible Causes
Increase mA till capture
Low battery
IABP removal
See IABP removal Hosptial Protocol on IntraNet.
References
Bojar, Robert M. (2011) Manual of Perioperative Care in Adult Cardiac Surgery. (5th edition).
DEVICES: LUMBAR DRAINS
1. Placed pre-operatively by cardiac anesthesia or Neuro IR if patient has
complex anatomy
2. Use “Lumbar Drain” order set
3. Post-operative lumbar drain management:
i. Zero the transducer at right atrium phlebostatic level
ii. Set the Transducer to 10mmHg
• Leave the stopcock closed to the transducer except when measuring
hourly pressure
• Keep the drain open to the patient to allow to continuous drainage
• When the ICP is above 10mmHg, the drain will act as a pressure
iii. Goal is to drain ~10mL/hr when ICP >10. Not to exceed drainage
of 20mL/hr
iv.
v. Maintain strict bed rest with HOB at 30 degrees or less while actively
draining
vi.
patient and reopen when destination reached.
4. For more information on ICP and prevention of spinal cord ischemia see
“Spinal Cord Ischemia page 50 under III. Post-operative Managament
DEVICES: TEMPORARY PACEMAKERS
Nomenclature
1st letter — chamber/chambers paced: A= atria, V= ventricle,
D- dual (atria and ventricle)
2nd letter — chamber/chambers sensed: A= atria, V= ventricle,
D- dual (atria and ventricle)
3rd letter — how the pacemaker responds to an event: I= inhibit, T- trigger
Temporary Pacing Techniques
Transvenous
Placed through introducer into the right ventricle. Routinely placed in TAVR pts
with Corevalves d/t increased risk for the development of heart block as the valve
continues to expand post deployment.
Transcutaneous
positions. Disadvantages include requiring higher pacing thresholds and patient
discomfort.
Epicardial Leads
The wires in the right subcostal region are atrial and in the subcostal
region are ventricular.
Minimally invasive valve surgeries the A and V wires will be in the same position.
Typically, a single ventricular wire (pacing lead) and a skin wire (ground) are
108 Procedures/Devices Procedures/Devices 109
Modes of Pacing:
Mode Advantages Disadvantages
AAI
Single lead
AV synchrony maintained
Able to assess ST changes
Unable to use in AF
Ventricular bradycardia may
occur in prescense of high
grade AV block
Instability of single atrial lead
Higher risk of thin atrial wall
VVI
Requires a single lead
Useful in prescense of AF and
high grade AV block
AV synchrony lost
Unable to assess ST changes
Loss of atrial kick
Risk of pacemaker syndrome
DDO
AV synchrony maintained
Use in AF and high grade AV
block
Heart rate responsive
Possible decreased
thrombotic events
Pacemaker mediate endless-
loop tachycardia possible
Pacemaker syndrome if
incorrectly set up
May not be able to assess ST’s
DDI
Uses two pacing leads (right
atrium and right ventricle) to
maintain minimum rate in
each cavity
Used in the presence of sinus
bradycardia with possible AV
conduction disorders or with
frequent atrial arrhythmia
Must feel comfortable setting
rate and AV node delay
For removal of temporary pacing wires, page 99 (section V, procedures, CT and
PW removal)
References: http://www.medtronic.com/us-en/index.html
DEVICES: ON Q PUMPS
Non-narcotic pain relief system designed to deliver local anesthetic to or near
the surgical site via catheters.
The epidural or intrathecal route uses small quantities of medication to
provide targeted pain relief via multiple holes along the infusion segment of
distribution.
Placed intra-operatively by the surgeon or APP for primarily patients receiving
anterior thoracotomy incisions
Placing the Catheter
1. Gently hold T-handle and remove protective guard.
2. Introducer Needle: Insert (bevel up) through the skin approximately 3-5 cm
from surgical site
3. Advance introducer to desired location for catheter placement. Introducers
with Luer lock may be connected to a syringe to aspirate or inject a bolus of
4. While holding T-handle 1, withdraw trocar 2 from sheath
Change battery
Attempt to reverse the polarity of the leads by swapping the position
of the metal leads into the pacemaker cord
Electrolyte abnormalities
Sensitivity
Sensing refers to the ability of the generator to detect (“see”) and recognize
the intrinsic impulses of the myocardial tissue and to appropriately respond
to what it detects.
Sensitivity setting is measured in millivolts.
Typical atrial 0.4 mV
Typical ventricular 2.0 mV
Programming a higher sensitivity (higher number) makes the pacemaker
less sensitive to intrinsic cardiac activity.
Programming a lower sensitivity (lower number) causes the pacemaker to be
more sensitive to intrinsic cardiac activity.
How to determine appropriate sensitivity setting:
1. Set rate at least 10 ppm below patient’s intrinsic rate.
2. Adjust output: Set OUTPUT to 0.1 mA (A OUTPUT for atrial threshold; V
OUTPUT for ventricular threshold).
3. Highlight SENSITIVITY (atrial or ventricular)
4. Decrease SENSITIVITY: Slowly turn MENU PARAMETER dial
5. Increase SENSITIVITY: Slowly turn MENU PARAMETER dial clockwise
This value is the sensing threshold.
6. Set SENSITIVITY to half (or less) the threshold value.
This provides at least a 2:1 safety margin.
7. Restore RATE and OUTPUT to previous values.
Trouble Shooting Sensitivity
Failure to sense is when the generator does not recognize the heart’s intrinsic
impulses.
Pacemaker not sensitive enough to patient’s intrinsic rhythm.
Increase the sensitivity by lowering the mV
Attempt to reverse the polarity of the leads by swapping the position of
the metal leads into the pacemaker cord
Low battery.
Malfunction of pacemaker or cable.
Over-sensing: Pacer sees too much (QRS, T wave, P wave and baseline)
Decrease sensitivity by increasing the mV
Checking underlying rhythm
Safest method is to slowly turn down the rate as opposed to disconnecting
the leads from generator or pausing the pacemaker as this gives time for the
patient’s native conduction system to emerge
110 Procedures/Devices Procedures/Devices 111
Sponge (item # 195925)
regular wound vac upon discharge
Discharging a patient home with Wound VAC
Ensure Case management is involved early to ensure insurance authorization
and supply delivery
If short term Vac therapy is needed, consider Vac Via
Can use placed on a patient for up to 4 days and then switched to wet-to-
dry dressings if Vac is no longer needed
Vac Tips:
Stanford Policy states wound Vac changes are to be done Monday,
Wednesday and Friday.
Use clinical judgment if wound vac was placed at an odd time. Product
Cut the sponge to the size of the wound or larger never smaller than the
wound so that the drape does not stick directly to the wound.
Cut a big hole for track pad at least the size of a quarter.
When placing Wound VAC in clinic:
If the VAC is a new placement- the patient will be Admitted to Observation for
wound vac placement and supply authorization via case manager (DO NOT
ADMIT VIA ED)
If the VAC is established- patient should bring own supplies from home for in
clinic changes
Prevena:
For use with closed incisions
Should be placed at the time of wound closure in the OR, can also be placed
later
The pump battery lasts for 7 days.
Dressing should be removed and wound checked prior to discharge
(even if before battery dies)
When the battery dies, the pump can be thrown away and the patient
removes the dressing and resumes normal wound care
Risk for poor wound healing criteria (i.e. use of provena should be
considered)
Obesity (BMI>36)
Diabetes (insulin-dependent, dialysis, or previous diabetic-induced
organ damage)
COPD (forced expiratory volume in 1 second < 80%)
Bilateral IMA take-down
COPD history
Corticosteroid use
Abnormally high preoperative creatinine ( > 90th percentile)
More intraoperative blood transfusions (3 or more)
Longer length of operation (>4 hrs.)
Previous known poor wound healing episode
5. Advance catheter through sheath until entire infusion segment is within
desired location
6. Coil catheter and secure with adhesive strips
7. Apply occlusive dressing over insertion site and coiled catheter. Keep
8. Connect catheter to pump tubing.
Post-operative period:
Pumps are not managed by pain service (do not page Pain service with
questions), they are managed by the primary team
The pump works by administering a continuous infusion of bupivacaine
locally at the site of the incision.
The pump is used in adjunct with analgesics (Tylenol, oxycodone, fentanyl,
dilaudid). While OnQ pump in place avoid concurrent use with other
similar agents, i.e. Lidocaine infusions
Medication order: Bupivacaine 0.25% in 270mL @ 2mL/hr
Removal:
medicine moving through the tubing. You may notice the outside bag on the
ball getting looser with wrinkles over time
The pump should be removed 24 hours before discharge to allow for time to
ensure adequate pain control using oral pain medications
To Remove: remove the dressing, remove small suture anchoring pump to
skin, and pull the clear catheter. The tube should come out easily. If it is hard
to remove or starts to stretch, stop and call your doctor right away.
The end of the tube should have a colored tip so you know that it is all
out. If the end of the tube does not have a colored tip, call your doctor
right away.
The entire unit should be disposed of in the red biohazard bins.
References: Clark, K. (2010). On-q catheters and introducers. ON-Q Pain Relief System. Retrieved
from http://www.halyardhealth.com/media/155090/14-60-603-0-04.pdf.
DEVICES: WOUND VAC
Vera o:
Preferred over regular wound Vac for inpatients (may heal area faster)
Normal saline is the solution of choice. Any topically approved solution
can be placed into the Vac
Typical Settings:
-125mmHg
0-20 min wash every 2-4 hours
Grey foam can be used for packing tunneling areas or undermining that is
hard to visualize
General principles:
When changing the Vac, use the pad to estimate how much saline is
Supplies needed (Central supply # 35047
1000mL container (item # 86309)
Cassette ( item #195927)
112 Reference Material Reference Material 113
SURGEON PREFERENCES
Surgeon
Preferences
Clinic
Woo
o Review all images and review surgical plan prior to clinic
o 2 week
Boyd
o Echo within 3-6 months for Valves
o Cath within 6 months (if CAD), within 1 year if most recent was clean/Valve
o CTa within 3-6 months for Ascending aorta
o Calculate STS score on all patients pre clinic (use most recent or normal
creatinine)
o Calculate Syntax score for all CAD patients
o All notes completed same day of clinic
thromboembolic event
For inpatient CABG consults— see Boyd Consult H&P document
Lee
o Calculate STS score on all patients pre clinic (use most recent or normal creatinine)
o Echo within 3 months
o Cath within 6 months (if CAD), within 1 year if most recent was clean/Valve
o CTa within 3-6 months for Ascending aorta
o CTa (vs CT L atrial mapping) needed for all patient with prior history of ablation/
MAZE
o If pacemaker, obtain make, model, implantation date
o Calculate STS score on all patients pre-clinic (use most recent or normal
creatinine)
o PFTs if any smoking history in last 10 years
o Carotid US if carotid bruit on exam, h/o prior TAI or stroke, age > 65, smoking
history, or family history of stroke
o Obtain bilateral LE duplex US if history of vein stripping
o All notes completed same day of clinic
o DO NOT HOLD ASA PRE-OPERATIVELY
o Post ops:
o MAZE:
o 1-month POV – need ECG during clinic visit (may need TTE if patient’s
most recent TTE prior to discharge had LVEF< 40%).
o 3-month POV -needs 72 hour Ziopatch as close to clinic visit as possible
and a TTE prior to visit.
o 6-month POV – needs 72 hour Ziopatch as close to clinic visit as possible.
o 12- month POV –needs 72 hour Ziopatch as close to clinic visit as possible.
o Annually with 72 hour Ziopatch. VALVE follow up at 1 mos with Echo,
then annually
o CABG fu at 1 mos (Echo only needed if EF decreased at discharge or
< 40% pre op)
o Aortic surgery patients: FU @ 1, 3,6, and 12 months with CT scan
Fischbein o Pre op
o No Tissue consent for Aorta patients
Miller
Hiesinger o Review all images and review surgical plan prior to clinic
SURGEON PREFERENCES, CONTINUED
Surgeon
Preferences
ICU Tele
Woo o DC labs early if able
o Post op CT c/a/p prior to discharge on
Acute Type A dissections only
o Ok to DC home same day PW removed
Boyd
o CABG patients 75mg Plavix daily x1
year
o All patients 200mg PO amio daily
o SubQ heparin for DVT prophylaxis
if no contraindication
o Endocrine consult to manage DM if
elevated A1c
o Daily senna started while in ICU
o FAST TRACK (all uncomplicated
CABG with normal EF)
POD #1:0600; Cordis/
Swan out by 1000 (even if still on
and Plavix
POD #2: Daily labs on case by case
basis. Transfer out of ICU
Overall considerations:
insulin gtt and start diet as early
as possible, ok to eat POD #0. Ok
to remove foley POD 1 even if on
diuretics. If waiting in ICU for tele
bed, ensure PT/OT and patient
mobilization.
o DC labs early if able
o CABG patients 75mg Plavix daily x1 year
o All patients 200mg PO amio daily for
o No Iron on discharge
o Remove PW prior to CT
o SubQ heparin for DVT prophylaxis if no
contraindication
o No imaging needed prior to discharge
o Acute Type A dissection post op CT @
1month follow up appointment
o Endocrine consult to manage DM if
elevated A1c
o For routine CABG, goal is discharge by
at least POD #5
o For myocardial bridge, DC Paravertebral
catheter POD #3 with goal of discharge
by POD #4
Lee o No IV amio gtt, boluses only
o No nicotine patch for CABG
o Avoid Reglan (due to black box
warning and association with
tardive dyskinesia)
o No IV amio gtt, boluses only
o No nicotine patch for CABG
o Coreg no better than metoprolol for
Heart failure patients
o For LAA excision: Inspra 25mg BID
o Avoid Reglan (due to black box warning
and association with tardive dyskinesia)
Fischbein o Do not wean inotropes without
discussing directly
o For patients on high dose pressors
or with high oxygen requirements,
discuss PO diet directly before
initiating
o For post op CABG patients,
continue NTG while on Epi if blood
pressure allows
o Start Epogen/Iron/Vit C in ICU for
post op anemia
o IV Lasix and KCL while inpatient
o Leave central line in place
o PW remain in place until day prior to
discharge
o Prior to discharge:
o Echo all valves
o CT all aortas (with 3D
measurements
o Must approve all discharges
o No IV hydralazine in dissections
o PW out prior to CT if possible
Miller o Avoid hydralazine in Aortic
Dissections/Aneurysm
o Prior to discharge:
o Echo all valves (once PW removed
and within 2kg pre op wt)
o CT all aortas (with 3D
measurements
o Must approve all discharges
o No IV hydralazine dissections
o For LAA excision: Inspra 25mg BID
Hiesinger o Post op imaging per patient- not
standard
114 Reference Material Reference Material 115
CARDIAC SURGERY PROCEDURE CLEARANCE
Dental Guidelines
Pre-op:
Dental clearance will be obtained by schedules via clearance letter
To be cleared for cardiac surgery:
Dental exam in last 6 months
No evidence of current dental infection or anticipated dental care needed
within the next 6 months (Excluding restoration or dentures)
Post-Op:
Patients with valve repair or CABG SHOULD NOT have dental cleaning or work
done for at least 3 months post-op.
material implanted SHOULD NOT have dental cleaning or work done for
at least 6 months post-op and should take prophylactic oral antibiotics,
prescribed from their dentist, before any procedures. (AHA guidelines)
Patients are encouraged to follow up with their cardiologist recommendation
before proceeding with dental work and regarding the need for prophylactic
antibiotics.
Colonoscopy/Sigmoidoscopy Guidelines
Post-Op:
Patients SHOULD NOT have an elective colonoscopy for at least 6 months
post op
Prophylactic antibiotics (usually IV given within 30 minutes of procedure)
should be considered for high risk patients only (presence of prosthetic heart
history of endocarditis)
Prophylaxis IS NOT recommended for patients with the following: isolated
ASD, ASD s/p repair with patch, post op CABG, valvar dysfunction, mitral valve
prolapse, presence of cardiac pacemaker
References:
Oliver, G., Lowry, A., Vernava, A., Hicks, T., Burnstein, M., et. Al. (2000). Antibiotics prophylaxis clinical
practice guideline: supporting documentation. The American Society of Colon and Rectal Surgeons.
PRE-OP: CHECK LIST
H&P
Completed within 24 hours of procedure
OR
Completed within 30 days, with H&P interval within 24 hours of
procedure
Consent (good for 1 year)
Procedure
ICU
Tissue/Study
Refusal of blood products if patient does NOT consent to blood
transfusion
Pre op labs/imaging (must be completed at Stanford within 30 days of
surgery)
CMP
PT, PTT
HgbA1c
Phosphorus
Urinalysis, screen for culture
Type and Screen (for outpatient, clot should be extended for 30 days.
For inpatient, must be within 72 hours of procedure)
RBCS (Refer to page 116 to know how many units to order ahead)
EKG
CXR (2V preferred)
Day of surgery orders (found in order set #4658):
Surgical preparation- clipping, antimicrobial showers x 2, Mepilex to
sacrum
Surgical prophylaxis with antibiotics (ON CALL)
Peridex mouthwash (ON CALL)
DVT prophylaxis
Misc pre op
Anticoagulation bridging with Lovenox
Radial artery harvest work up
Dental clearance
Any other studies needed (Cath, Echo, CT, etc)
TAAA Repair specic:
Patients are pre-admitted day before surgery for lumbar drain, epidural, and
bowel prep.
Page pain service to place epidural preferably day before it is needed
(2-PAIN)
Clear diet
Bowel prep
116 Reference Material Reference Material 117
PRE-OP:CARDIAC SURGERY PATIENT BLOOD
MANAGEMENT PROGRAM
(Ref: Info redistributed from CV Clinical Outcomes; 2011: Stanford Maximum Surgical
Blood Order Schedule (MSBOS) Criteria)
Procedure: Type & Screen and
Type & Cross (Y/N)
Cardiac Surgery
recommended # RBC
units order pre-op
Combo Sx: “Low Risk” Group:
(Includes: Iso CABG, Open & Mini Valve Repair/Replace)
1st Sx: IsoCABG
Y 2
1st Sx: Open AVR
Y 2
TAVR (TFem, TApical,
TAortic)
Y 4
1st Sx: Valve + CABG OR
Multiple Valves
Y 4
1st Sx: AoRoot (no arch)
Combo TD, CVG, AscAo
Y 4
1st Sx: TD +/- Asc Arch
Y 4
1st Sx: CVG +/- Acs Arch
Y 4
1st Sx: Asc + Arch (no valve)
+/- descending
Y 4
Redo Sx: CABG + Valve
Y 4
Combo Sx: “High Risk” Group:
(Includes: Redo TD, Redo CVG, any 1st or Redo Arch Replace, Open Desc Ao,
and 1st or Redo TAAA)
Redo Sx: TD +/- Arch
Y 6
Redo Sx: CVG +/- Arch
Y 6
Redo Sx: CVG, No Arch
Y 6
Redo Sx: Asc +/- Arch
Y 6
Open Desc. Ao (All)
Y 6
Open TAAA (All)
Y 6
*Key:
TD= Tyrone David (aka: David V, Valve Sparing)
Patients with Heparin allergy or HIT; document in H&P note and inform perfusion on
surgical day. (Patient with Heparin allergy will receive Argatroban, Bivalirudin
or heparin.)
Pre-Op Blood Saving:
Autologous Donation: Patients can donate their own blood, can donate 6
weeks before surgery, increase folic acid, vitamin C, iron supply (ask your
attending surgeon if this is preferred)
Jehovah’s Witness: Patients Witnesses’ refusal of transfusions of whole
blood or its four primary components—red cells, white cells, platelets and
plasma; can use use of fractions such as albumin, immunoglobulins and
hemophiliac preparations & cell saver. (WatchTower Society)
Bloodless medicine program in process 1/2017. Refer to updated protocol
for current pre-operative guidelines for patients who refuse blood
transfusion.
Herbal Products: Potential interactions to avoid (JACC, 2010), (Alfalfa,
Angelica, Bilberry, Garlic, Ginger, Ginko, Ginseng, Echinacea, Licorice, St.
Johns Wart). Can cause interactions with cardiac medications & increase
bleeding during surgery.
Intra-Op Blood Saving:
Blood clotting agent/blood derived fraction agents (Coseal/Tisseal/Floseal)
Perfusion:
Cell Saver: recovering blood lost during surgery and re-infusing it into
the patient. It is a major form of autotransfusion. Cell processors are
red cell washing devices that collect anticoagulated shed or recovered
blood, wash and separate the red blood cells (RBC) by centrifugation, and
reinfuse the RBC.
PRE-OP: CLASSIFICATIONS
CCS Functional Classication of Angina
Class Description
Class I Angina only during strenuous or prolonged physical activity
Class II Slight limitation, with angina only during vigorous physical activity
Class III Symptoms with everyday living activities (i.e. moderate limitation)
Class IV Inability to perform any activity without angina or angina at rest
(i.e. severe limitation)
Staging Kidney Disease: always document CKD Stage 3 or greater
Stage Description
Stage I With normal of high GFR (GFR > 90mL/min)
Stage II Mild CKD (GFR = 60-89mL/min)
Stage IIIa Moderate CKD (GFR = 45-59mL/min)
Stage IIIb Moderate CKD (GFR = 30-44mL/min)
Stage IV Severe CKD (GFR = 15-29mL/min)
Stage V End Stage CKD (GFR < 15mL/min)
GFR calculator Website:
http://www.davita.com/gfr-calculator/
http://www.kidney.org/professionals/KDOQI/gfr_calculator
118 Reference Material Reference Material 119
ACC/AHA Classication of CHF
The ACC/AHA created four classications from risk for develop the
disease to severe disability.
Stage Description
A (High risk for
developing CHF)
Hypertension, DM, Family history, CAD
B (Asymptomatic HF) Previous myocardial infarction (heart attack), valvular
C (Symptomatic HF) Structural heart disease, fatigue, low tolerance level for
physical activity
D (Refractory
end-stage HF)
Severe limitations. Experience symptoms even
while at rest.
NYHA Functional Classication
The NYHA classied heart failure into classes base on functional
limitations and severity.
Class FUNCTIONAL CAPACITY: Patient Symptoms
I (Normal) Few observable sx, no limitations in ordinary physical activity
II (Mild) Mild observable sx and slight limitation during ordinary activity.
Comfortable at rest.
III (Moderate) Marked limitation in physical activity due to symptoms even
during less than ordinary activity. Comfortable only at rest.
IV (Severe) End-stage heart failure. Severe limitations. Experience
symptoms even while at rest.
Class OBJECTIVE ASSESSMENT
A No evidence of cardiovascular disease. No symptoms and no
limitation in ordinary physical activity.
B Objective evidence of minimal cardiovascular disease. Mild
symptoms and slight limitation during ordinary activity.
Comfortable at rest.
C Objective evidence of moderately severe cardiac disease.
Marked limitation in activity due to symptoms, even during less
than ordinary activity. Comfortable only at rest.
D Objective evidence of severe cardiovascular disease. Severe
limitations. Experiences symptoms even while at rest.
For Example:
A patient with minimal or no symptoms but a large pressure gradient across the
Function capacity I, Objective Assessment D
A patient with severe angina syndrome but angiographically normal coronary
Functional Capacity IV, Objective Assessment A
Other Helpful Scores/Resources
NYHA Class
Website:
http://www.heart.org/HEARTORG/Conditions/
HeartFailure/AboutHeartFailure/Classes-of-Heart-
Failure_UCM_306328_Article.jsp
Griepp Score The 1997 ATS paper by Randy Griepp and colleagues
describes an easy-to-use risk of rupture calculator
developed by Abe DeAnda (Chief Resident 2000-
2001). If aortic dissection, RBG just adds 0.5 cm to
the descending thoracic aortic and abdominal aorta
diameter numbers. Several other calculator tools are
also on the spreadsheet.
Reference the
Cardiac Surgery
APP Shared Box
folder for this
information.
Syntaxcore SYNTAX score II creates accurate mortality predictions
to guide the choice between PCI and CABG for
patients with multivessel coronary disease.
http://
syntaxscore.
com/
PRE-OP: NORMAL ECHO VALUES
Normal Echo Values
LV Diastolic Dimension 3.7-5.5cm
LV Systolic Dimension 2.0-4.0 cm
Interventricular septum (Diastole) 0.6-1.1 cm
LV Posterior Wall (Diastole) 1.8-2.2 cm
LVOT Diameter (Systole) 1.8-2.2cm
Aortic Root (Diastole) 2.0-3.7cm
2.0-4.0cm
<20cm2
16-28ml
RV Diastolic Dimension 0.9-2.5cm
Pulmonic Valve Echo Values
Mild 5-25mmHg
Moderate 25-49mmHg
Severe >50mmHg
Aortic Valve Echo Values
AS Grading Mean Gradient
(mmHg)
Peak Velocity (m/s) AVA (cm2)
Normal < 10 < 2.6 >2.5
Mild 10-25 2.6-2.9 1.5-2.5
Moderate 20-45 3.0-4.0 1.0-1.5
Severe >45 >4.0 0.7-1.0
Critical >50 >4.0 <0.7
AR Grading Central Jet width* Regurgitant Volume
(per beat)
EROA (eective
Regurgitant oriace
area)
Mild < 25% of LVOT width < 30mL <0.1cm2
Moderate 25-65% of LVOT width 30-59mL 0.1-0.3cm2
Severe >65% of LVOT width >60mL >0.3cm
Tricuspid Valve Echo Values
Signicant tricuspid stenosis
Mean pressure gradient >/= 5mmHg
Valve area </= 1cm2
Tricuspid
Regurgitation
MILD MODERATE SEVERE
Jet area < 5 5-10 >10
RV/RA/IVC Size Normal Normal or dilated Usually dialates
120 Reference Material Reference Material 121
Mitral Valve Echo Values
MS grading Valve Area Mean gradient Pulmonary artery
pressure (mmHg)
Mild >1.5 cm2 <5mmHg <30mmHg
Moderate 1.0-1.5 cm2 5-10mmHg 30-50mmHg
Severe <1.0cm2 >10mmHg >50mmHg
MR grading Jet area Regurgitant Volume EROA (eective
Regurgitant oriace
area)
Mild <20% of LA area <30mL <0.2cm2
Moderate 20-40% of LA area 30-59mL 0.2-0.39
Severe >40% of LA area >60mL >0.40cm2
PRE-OP: OBTAINING CONSENT/PROCEDURE LIST
Procedure Correct verbiage for Consent
CABG
• Does not need to include IMA (LIMA/RIMA)
Consent must specify conduit harvesting when applicable:
EVH= Endoscopic vein harvest
RAH= Endoscopic radial artery harvest
CABG
MIDCAB
possible sternotomy, cardiopulmonary bypass on standby
TAVR Transcatheter aortic valve replacement
• Include approach (transfemoral, transapical, or transaortic)
• Also include cardiopulmonary bypass on standby
• Also include transesophageal echocardiogram
Mini MVR Right anterior thoracotomy; mitral valve/replacement repair on
cardiopulmonary bypass, possible sternotomy.
Mini AVR Minimally invasive aortic valve repair/replacement; on cardiopulmonary bypass
Hybrid MAZE Bilateral video assisted thoracoscopy; pulmonary vein isolation; with additional
MAZE; cardiopulmonary bypass on standby
Cox Maze Maze procedure on cardiopulmonary bypass
Myectomy/
Myotomy
Myectomy/myotomy with possible mitral valve repair/replacement on
cardiopulmonary bypass
Myocardial bridge
Redo stern Redo sternotomy
LAA Excision
Laser lead
extraction
Laser lead extraction with possible pacemaker generator change; possible
sternotomy; Cardiopulmonary bypass on standby
TEVAR (CT surgery
attending is
surgical consent
attending, Dr. Dake
does not sign this
procedure consent)
• Do not include Lumbar drain (Anesthesia will consent separately)
VSARR or Tirone
David (T-David)
Valve sparing aortic root replacement, possible aortic valve replacement on
cardiopulmonary bypass
Aortic replacement Include following when applicable: ascending aortic replacement, descending
aortic replacement, total arch replacement, hemi-arch replacement, elephant
Aortic root Aortic root replacement including aortic valve replacement on cardiopulmonary
bypass
TAAA Thoracoabdominal aortic aneurysm repair on cardiopulmonary bypass
SACP & PHCA Under Deep Circulatory Arrest
Heart transplant Heart transplant on cardiopulmonary bypass
VAD Ventricular assist device insertion on cardiopulmonary bypass
• Include type of device: Heartmate II or Heartware
Procedure consent must be signed by someone who can perform the
procedure listed
Ex: Valve replacement = Attending/resident
Ex: Cardioversion/Pigtail placement = APP
ICU consent can be signed by APP
Consent is good for 1 year
Make sure all abbreviations are completely spelled out. NO ABBREVIATIONS.
Check blood consent box on both forms and give patient transfusion packet (If
the patient refuses blood transfusion, use the additional blood refusal form)
Median sternotomy DOES NOT need to be included on expected “standard
sternotomy” consents. ONLY on “Possible Sternotomy” cases (i.e. anterior
thoracotomy, then “possible sternotomy” should also be included).
NO SCRATCHES, CROSS THROUGHS, OR SCRIBBLES ALLOWED ON CONSENT
PRE-OP: PFT AND CAROTID US INTEPRETATION
Carotid Duplex Ultrasound Criteria for Grading Internal Carotid Artery Stenosis
Degree of
Stenosis (%)
ICA PSV (cm/2) ICU/CCA PSV
Ratio
ICA EDV (cm/2) Plaque Estimate
(%)
Normal < 125 <2.0 <40 None
<50 <125 <2.0 <40 <50
50-69 125-230 2.0-4.0 40-100 >50
>70 to less than
near occlusion
>230 >4.0 >100 >50
Near occlusion High, low, or not
detected
Variable Variable Visible
Total occlusion Not detected Not applicable Not detected Visible, no lumen
*Plaque estimate (diameter reduction) with gray scale and color Doppler ultrasound. ICA = internal
carotid artery; CCA= common carotid artery; PSV = peak systolic velocity; EDV = end- diastolic velocity
*Intervention may be required prior to cardiac surgery on cardiopulmonary bypass if degree of
stenosis is > 90% unilateral or > 75% bilateral due to increased stroke risk
Normal Value of Pulmonary Function Tests
** FEV1 80% to 120%
FVC 80- 120%
Absolute FEV1/FVC ratio Within 5% of the predicted ratio
TLC 80-120%
FRC 75-120%
RV 75-120%
** DLCO
Also known as TLCO or Dsb
>60% to <120%
**These are key for interpreting
Spirometry
Low FEV1/FVC
Obstruction
Bronchodilator
FEV1 unchanged/
partially
improved
(asthma or COPD)
Obstruction
Normalizes
(asthma)
DLCO
Low (COPD/
Emphysema/
bronchiolitis)
Normal/High
(asthma or COPD)
Normal
? Asthma
Bronchoprovocation
challenge
FEV1
Decreased
(asthma more
likely)
No Change in FEV1
(asthma unlikely)
DLCO
Low (anemia,
early ILD,
pulmonary
vascular
disease)
Normal/
High
Normal
Normal FEV1/
FVC
Low VC
Restriction
Confirm with
lung volumes
DLCO
Low
(ILD)
Normal (chest
wall/
neuromuscular)
Maximum
inspiratory/
expiratory
pressures
Low
(neuromuscular)
122 Reference Material Reference Material 123
PRE-OP: PERIPROCEDURAL
ANTICOAGULATION BRIDGING
Brand Name
(Generic Name) Half Life/Onset of Action Last dose of medication Before Surgery:
If indicated: When To Start Lovenox
(dosing=1mg/kg)
#
syringes
Notes Cath procedures
Coumadin
(Warfarin)
Once daily dosing
20-60hours/3-5 days 5 days before date of surgery
Start 2 days after d/c coumadin (inj Q12 until day
before surgery. Day before surgery just ONE
injection in the morning)
5
Example: surgery date 4/10; last dose
Coumadin 4/5; off all one day, 4/6; start
Lovenox Q12 on 4/7; last Lovenox injec on
4/9 (morning before sx)
Hold 5 days prior for femoral access,
and if pt mod-high risk for clot bridge
to Lovenox. Hold 2 days prior for
radial access
Eliquis
(Apixaban)
BID dosing
9-14hours/3-4 hours
5 days before date of surgery
(If CrCl < 50 Hold 6-7 doses)
Start 1 day after d/c anticoagulant (inj Q12 until day
before surgery. Day before surgery just ONE
injection in the morning)
7
Example: surgery date 4/10; last dose
Eliquis 4/5(am); start Lovenox Q12 on 4/6;
last Lovenox injec on 4/9 (morning before
surgery)
Hold x 2 days: the day before and
the day of Cath
Xarelto
(Rivorxaban)
Once daily dosing
11-13 hours/2-4 hours
3 days before date of surgery
(If CrCl < 30 Hold 3 doses)
Start 1 day after d/c anticoagulant (inj Q12 until day
before surgery. Day before surgery just ONE
injection in the morning)
3
Example: surgery date 4/10; last dose
Xarelto 4/7(am); start Lovenox Q12 on 4/8;
last Lovenox injec on 4/9 (morning before
surgery)
Hold x 2 days: the day before and
the day of Cath
Pradaxa
(Dabigatran)
BID dosing
12-17hours /1 hour
5 days before date of surgery
Start 1 day after d/c anticoagulant (inj Q12 until day
before surgery. Day before surgery just ONE
injection in the morning)
7
Example: surgery date 4/10; last dose
Pradaxa 4/5(am); start Lovenox Q12 on
4/6; last Lovenox injec on 4/9 (morning
before surgery)
Hold the night before and morning of
procedure. Last dose will be in the
morning the day before Cath
SAVAYSA
(endoxaban)
Once daily dosing
10-14 hours/ 1-2 hours
3 days before date of surgery
(If CrCl < 30 Hold 3-4 doses)
Start 1 day after d/c anticoagulant (inj Q12 until day
before surgery. Day before surgery just ONE
injection in the morning)
3
Example: surgery date 4/10; last dose
Savaysa 4/7( AM); Lovenox BID 4/8 1
lovenox inj AM only on 4/9.
Hold x2 days: the day before and the
day of Cath
Plavix (Clopidogrel)
5 days before date of surgery
Start 1 day after anticoagulant held (inj Q12 until
day before surgery. Day before surgery just ONE
injection in the morning)
7
Only bridge for pt's taking Plavix for A.fib.
If taking for Stents, hold 5 days before
surgery and do not bridge
PLETAL (cilostazol)
11-13 hours, reach steady state blood
levels within a few days.
5 days before date of surgery Does not need bridging
Asprin
If having valve surgery d/c 2 days before surgery date.
If having CABG stop day before
Does not need bridging
If taking ASA 325mg, have patient
decrease dose to 81 mg as soon as
procedure scheduled
EFFIENT (prasugrel)
7 hours /4 hours 5-7 days before date of surgery Does not need bridging
Pre operative bridging with lovenox is required for all mechanical heart valves* & is only need for atrial fibrillation when CHAD score is High** . For low clot risk, hold anticoagulant per chart above.
Medications to CONTINUE
to take morning of surgery
Medications to STOP before surgery
CHADS SCORE
Lovenox to Coumadin
Anti-seizure meds
ASA:
Valve Surgery= Last Dose 2 days before surgery
CABG only: Stop day before surgery CABG &
Valve=Stop day before surgery (Please follow
attending preference if different)
1 pt for each risk factor present:
CHF, HTN, DM, PAD or MI, Age 65-74,
Female
2 pts for each risk factor present
:
Age > 74 years old, Prior stroke or TIA or
thromboembolism
1. Resume oral
anticoagulant and
lovenox evening after
procedure if no bleeding
2. Resume oral
anticoagulant + lovenox
post procedure day 1-3
Anti-Psych meds
Blood Thinners: see above
SCORE / RISK**
Beta-blockers
NSAIDS: stop 7 days before surgery
0-2 = LOW
Depression meds
Insulin: Insulin Am dose is normal the day before
surgery. Insulin PM dose is
½ dose the evening before
surgery. Nothing on the morning of surgery
3-4 = MODERATE
Inhalers
Metformin; stop 48 hours before surgery
5-6 = HIGH
Immunosuppressive meds
Stop ALL vitamins;1 week prior to surgery
TIA IN PREVIOUS 3 MONTHS = HIGH
Methadone
Fish oil; stop 5 days before surgery
SEVRE VALVULAR DISEASE = HIGH
Nitrates; (Imdur)
Herbs; stop asap (many of these have anti-coag effects)
Parkinson's meds
Maltaq (dronedarone); DO NOT take day of surgery,
last dose is day before surgery.
Proton Pump Inhibitors (PPI's)
*If Presence of Mechanical Mitral valve: References:
Thyroid meds
Birth Control Pills
1. Last dose coumadin 7 days prior to surgery
2. Bridge with lovenox as above
3. Admit to observation day prior to surgery for
heparin drip (to be stopped 6 hours before
surgery).
Pernod, G., Godier, A., Gozalo, C.,
Tremey, B., Sie, P. (2010). French clinical
practice guidelines on the management of
patients on vitamin K antagonists in at-risk
situations (overdose, risk of bleeding, and
active bleeding). Thrombosis Research,
126, e 167-e174.
Brunett, A.E., Mahan, C.E., Vaquez,
S.R.,Oertel, L.B., Gardcia, D.A., &
Ansell, J. (2016) Guidance for the
practical management of direct oral
anticoagulants (DOACs) in VTE
Treatment. Journal of Thromb
Thrombolysis, 41 : 206-232.
Last updated 12/2016
Pre-procedure Anticoagulation Bridging Recommendations
for Cardiac surgery
3. Check INR post
proceudre day 4 and DC
lovenox if INR theraputic
POST-OP: IMAGING
Modality Inpatient Contact Info Misc
Echocardiogram
(viewed in Xcelera)
Scheduling: 5-4160, 5-4159,
3-8988
Reading room: 3-9503
o Use TAVR or TMVR echo order when
appropriate
CT (+/- angio) scan
(viewed in Centricity)
Scheduling: 3-6885
Body reading room: 4-9617
CVI reading room: 6-2424
Chest reading room: 3-1346
Neuro reading room: 4-3145
o Gated: evaluates coronaries (Note
comments)
o Pre and post op aortic disease
include in comments: Please
perform with 3D measurements
and images for treatment
planning and surveillance (use
smart phrase CTANGIO3DIMAGES)
mapping) used for pre-op Maze
o Consider need for CT chest vs CT
Chest/Abdomen/Pelvis
CT CORONARY ANGIO
(viewed in Centricity)
Scheduling: 3-6885
CVI reading room: 6-2424
o Limited study- concentrated on heart
and coronary arteries (does not
include thoracic aorta)
o Will always be completed gated
in comments. If patient is in atrial
MRI (viewed in
Centricity)
Scheduling: 3-6855
Body reading room: 6-8591
Cardiac reading room:
6-2424
Neuro reading room:4-3145
Vascular lab: 5-5227
o For Aortic Disease, include comment:
Please perform cardiac MRI (gated)
with cross hatching, refer to Dr.
Fleishman if unsure of protocol.
US Carotid
(viewed in Centricity)
Vascular lab: 5-5227
Spirometry with DLCO
(results in Epic)
Inpatient: 3-6371
Adult pulmonary clinic:
5-7061
o PFTs can be performed by Inpatient
beside respiratory therapist (during
FDG PET CT Clinical
Cardiac Viability with
resting myocardial
perfusion scan (viewed
in Centricity)
Scheduling: 3-6885
Body reading room: 4-9617
CVI reading room: 6-2424
Chest reading room: 3-1346
o Include in comments: testing
myocardial viability in CAD patient as
pre-op work up for CABG
Venous Ultrasound
(viewed in Centricity)
Scheduling: 3-6855
Reading room: 8-2401
Arterial Exam/ABIs in
Vascular clinic (viewed
in Centricity)
Vascular lab: 5-5227
Tagged WBC scan
(viewed in Centricity)
Nuclear Med scheduling:
4-4278
Nuclear Med reading room:
8-2414
Nuclear Med techs: 4-5684
o Nuclear- bone
Cardiac cath
(viewed in LifeImage)
Cath lab extension: 3-7676
Cath lab recovery: 3-9317
o To schedule inpatient, page
interventional cardiologist on call
EKG lab 3-7121
1-4987
o Places long term cardiac monitors on
discharge
X-ray 62198
Scheduling: 37030
Reading room: 87996
Endoscopy 5-8117
124 Reference Material Reference Material 125
POST-OP: ABG INTERPRETATION
pH / pCO2 / paO2 / Sat % / Base Decit / Bicarb
Normal range 7.35 – 7.45
< 7.35 Acidosis
• Look at pCO2
o If High
respiratory acidosis
o If normal
metabolic acidosis
• How to Fix it:
o Respiratory acidosis:
• Intubated: increase RR, tidal volume to
increase minute ventilation
• Extubated: decrease sedation, Bipap to
increase ventilation
o Metabolic acidosis:
• Bicarbonate supplementation
• Further workup for source: Fluid status,
BMP, lactate, etc
> 7.45 Alkalosis
• Look at pCO2
o If Low
respiratory alkalosis
o If Normal
Metabolic alkalosis
• How to Fix it
o Respiratory alkalosis:
• If intubated: decrease RR, tidal volume
• If extubated: control pain, anxiety,
cause of hyperventilation (hypoxia?)
o Metabolic alkalosis:
• Further workup for source: BMP, PRBC
transfusion, overdiuresis, etc
pCO2 Normal range: 35-45
pCO2 < 35 Respiratory alkalosis
• See pH box (Alkalosis)
pCO2 >45 Respiratory acidosis
• See pH box (Acidosis)
Base Decit normal: +/-2 mEq/L; Bicarb normal 22-30
This is calculated, not measured on the ABG
Metabolic Acidosis:
• See pH box (Acidosis) above
Metabolic Alkalosis: high bicarbonate, positive base excess
• See pH box (Alkalosis) below
PaO2 Normal range 60-200mmHg; Sat % Normal range 92-100%
Increasing O2 content
• Increasing FiO2
• Increasing NC LPM
CXR/Ultrasound to assess for
• Pneumothorax
• Hemothorax
• Pneumonia
Increase PEEP (on ventilator or CPAP/BiPap) for
alveolar recruitment
Mobilize secretions:
• Chest PT
• Suctioning
• Mucolytics (ie Mucomyst)
Improve VQ matching
• Inhaled bronchodilators (albuterol)
• Inhaled vasodilators (Flolan, iNO)
• IPPV, incentive spirometer, acapella for
alveolar recruitment
• Consider stopping potential shunting
agents inhibiting hypoxic vasoconstriction:
Clevidipine, Nicardipine, Nitroprusside, NTG,
POST-OP: ADVANCED HEMODYNAMIC
MONITORING & PULMARY ARTERY CATHETERS
Parameter Normal Value
Cardiac Output (CO) 4-8 L/min
Cardiac Index (CI) 2.2-4 L/min/m2
CVP (central venous pressure aka Right atrial pressure) 3-8 mmHg
PA (pulmonary artery) Pressure Systolic 15-30 mmHg (PAS)
Diastolic 5-12 mmHg (PAD)
Mean 9-16 (PAM)
PCWP (pulmonary capillary wedge pressure) 4-12 mmHg
PVR (pulmonary vascular resistance) 37-250 dynes/sec/cm5
RV (right ventricular) Pressure Systolic 15-30 mmHg
Diastolic 3-8 mmHg
SVR (systemic vascular resistance) 800-1200 dynes/sec/cm5
Preload:
Decreased volume, decreased preload
Increased volume, increased preload which may increase MAP and CO
Aerload: the resistance that the heart has to overcome, during every beat, to
Cardiac index: the volume of blood pumped by the heart, per minute, per meter
square of body surface area. Cardiac Output = HR x Stroke Volume
Increased CO/CI: high circulating volume, increased strength of contraction,
early septic shock, vasodilatory state
Decreased CO/CI: hypovolemia or decrease in ventricular strength of
contraction
CVP: used to approximate Right Ventricular End Diastolic Pressure and assesses
Low CVP: hypovolemia, decreased venous return
High CVP: hypervolemia, right sided heart failure, tamponade
Mean Arterial Pressure (MAP): Arterial pressure in the vessels perfusing organs.
systemic vascular resistance (SVR). MAP = [(2 x diastolic)+systolic] / 3
Low MAP: hypovolemia, low cardiac output, or low SVR
High MAP: hypervolemia, high cardiac output, or high SVR
Systemic Vascular Resistance (SVR): measurement of impedance or resistance
Increased SVR: hypothermia, vasoconstrictors, hypovolemia, low cardiac
output state
Decreased SVR: hyperthermia, vasodilators, acidosis, early septic shock
Parameters for RV Function/Failure: used in context of overall clinical picture
Step-up: mean PA pressure – CVP
>10: adequate RV function
< 10: concern for RV dysfunction
PAPi: pulmonary artery pulsatility index = (PA Systolic – PA Diastolic) / CVP
>2: adequate RV function
1-2: at risk for RV failure
< 1: RV failure
126 Reference Material Reference Material 127
Figure 1 PA Catheter Waveforms
Pulmonary Artery Pressure (PA Pressure): Blood pressure in the
pulmonary artery
Pulmonary Vascular Resistance: measurement of impedance or resistance of
Increased PVR: hypoxia, hypercapnia, pulmonary vascular disease, PE
Pulmonary Capillary Wedge Pressure (PCWP): used to approximate LVEDP
High wedge pressure: LV failure, tamponade (cardiac compression), or
volume overload
Management of Hemodynamic Derangements
MAP CVP CO/CI SVR Treatment approach
Volume
Normal Normal Diuretic
Inotrope
Vasodilator
Inotrope/Vasodilator/IABP
Normal Vasoconstrictor
References:
PA Catheter Waveform image: https://www.studyblue.com/notes/note/n/hemodynamic-monitoring/
deck/3727974
Bojar, RM. (2011) Manual of perioperative care in adult cardiac surgery. (5th edition).
POST-OP: COMMON ICU DRIPS
Inotropes/Vasopressors
Receptor Location Action
Alpha Adrenergeic Vascular walls
also found in the heart
Vasoconstriction
Increase duration of
contraction
Beta 1 Adrenergic Heart Increase inotropy and
chronotropy, minimal
vasoconstriction
Beta 2 Adrenergic Blood vessels vascular and nonvascular
smooth muscle relaxation
Dopamine renal, splanchnic
(mesenteric), coronary, and
cerebral vascular beds
vasodilatation
Drug Mechanism of Action Dose Side eects
Epinephrine potent beta-1 adrenergic receptor activity
moderate beta-2 and alpha-1 adrenergic
0.01-.2 mcg/
kg/min
Increases heart rate
Can induce
tachyarrhythmias and
ischemia
Dopamine 1 to 2 mcg/kg per minute
• Selective vasodilatation of renal,
mesenteric, cerebral, and coronary beds
• may increases urine output d/t
and by inhibiting aldosterone and renal
tubular sodium
5 to 10 mcg/kg per minute
• stimulates beta-1 adrenergic receptors w/
increased cardiac output (stroke volume)
• mild alpha adrenergic receptor activation
increases SVR
>10 mcg/kg per minute
• stimulation of alpha-adrenergic receptors,
causing vasoconstriction with an increased
SVR
1-20mcg/kg/
min
tachycardia, arrhythmias
mcg/kg/minute
Milrinone Selective phosphodiesterase (PDE) inhibitor
in cardiac and vascular tissue, resulting in
vasodilation (pulmonary and systemic) and
increased inotropy with little chronotropic
activity.
.1-.5mcg/kg/
min
Caution
with renal
impairment
May cause peripheral
vasodilation,
hypotension, and/or
ventricular arrhythmia
Dobutamine Stimulates beta-1 adrenergic receptor,
increases inotropy and chronotropy and
2 to 20 mcg/
kg/minute
Can cause hypotension
Vasopressin Increases cyclic adenosine monophosphate
(cAMP). Direct vasoconstrictor without
SVR & MAP
.01-.04 units/
min
May decrease stroke
volume and cardiac
output in myocardial
dysfunction or precipitate
ischemia in coronary
artery disease.
Norepinephrine Stimulates both alpha-1 and beta-1 adrenergic
receptors; potent vasoconstriction & modest
increase in cardiac output
1-20mcg/min
Phenylephrine Pure alpha-adrenergic agonist. Causes
vasoconstriction with minimal cardiac inotropy
or chronotropy.
10-300mcg/
min
May decrease stroke
volume and cardiac
output in patients with
cardiac dysfunction
Isuprel Stimulates beta-1 adrenergic receptors.
Inotropic and chronotropic agent
1-10 mcg/min
adrenergic receptor
causes vasodilation and a
decrease in MAP
128 Reference Material Reference Material 129
Vasodilators
Drug Mechanism of Action Dose Side eects
Clevidipine Calcium channel blocker, ultra short-acting
selective arteriolar vasodilator, reduce
pressures or causing
1-16 mg/hr Pulmonary shunt
physiology and hypoxia
from inhibition of hypoxic
vasoconstriction
Nicardipine A short-acting calcium channel blocker 2.5-15mg/hr Contraindicated in
severe AS
Sodium
Nitroprusside
An arterial and venous vasodilator that
immediate onset of action
0.1- 3mcg/
kg/min
Prolong use (>72hrs) and
high dose (>3mcg/kg/
min) can cause cyanide
and thiocyanate toxicity
Nitroglycerine A direct vasodilator, primarily venodialtor,
arteriodilator at high dose.
Adjunct therapy for HTN
0.1-2 mcg/
kg/min
Esmolol
blocking agent
Dose: 25-
300mcg/kg/
min
Large volume infusion,
may contribute to volume
overload
Labetalol
Blocker.
0.5-3 mg/min
Hydralazine A direct-acting arteriolar vasodilator 10-20mg IV
push
Avoid in patients with
ischemic heart disease
and dissecting aneurysm
POST-OP: COMMON PO MEDS
Beta Blockers
Drug Usual Dose Misc Info
Atenolol 25-50mg PO qd Beta 1 selectivity, better for HR control
Metoprolol 2.5-100mg qD Beta 1 selectivity, better for HR control
Toprol XL 25-100mg qD Beta 1 selectivity, better for HR control
Avoid long acting BB in ICU, choose short acting
for easier titration.
Carvedilol 3.125-25mg BID Beta and Alpha blockage, better for Systolic HF
Labetolol 100-400mg PO QID Beta 2 and Alpha blockade
Nevibolol (Bystolic) 5-40mg PO qD Beta 1 selectivity
Beta Calcium Channel Blockers
Drug Usual Dose Misc Info
Dihydropryidines: potent vasodilators, little or no eect on contractility or conduction
Amlodipine 2.5-10mg PO qD Mainly for HTN & angina
Nicardipine 20-40mg PO TID Mainly for HTN & angina
Nifedipine 10-30mg PO/SL TID Mainly for HTN & angina
Non dihydropryidines: eect cardiac contractility and conduction
Diltiazem 30-60mg PO TID
180-360mg qD if long acting
Heart rate control/HTN
Verapamil 80-160mg PO TID Useful for angina
Nitrates
Drug Usual Dose Misc Info
Isosorbide
mononitrate (Imdur)
20mg PO qD Watch for Headache
Isosorbide dinitrate
(Isordil)
5-40mg PO TID Watch for Headache
Nitropaste 1-3 in q3-4 hr Watch for Headache
ACE inhibitors
(Avoid in acute renal dysfunction, adjust dose for moderate renal failure)
Drug Usual Dose Misc Info
Losartan (Cozaar) 25-100mg PO qD or in 2 divided
doses
Valsartan (Diovan) 80-160mg PO qD
Irbesartan (Avapro) 150-300mg PO qD
Cadesartan (Atacand) 8-32mg PO qD or in 2 divided
doses
Alpha Blockers
Drug Usual Dose Misc Info
Alpha 1 antagonist
Doxazosin (Cardura) 1.0-8mg PO qD Good for BPH
Prazosin (Minipress) 1.0-7.5mg PO BID
Terazosin (hytrin) 1-20mg PO qD Good for BPH, Slows HR, watch for
orthostatic h0tn
Alpha 2 antagonist
Clonidine (Catapres) 0.1-0.3mg PO BID Slows HR, good for nicotine withdrawal sx.
Rebound tachycardia/hypertension if stopped
Antiarrhythmics
Drug Usual Dose Misc Info
Amiodarone 400mg PO TID, wean to
200mg qd
Class III, prolongs action potential duration
Digoxin 0.125-0.25mg PO qd Leads to increased contractility through inhibition
of the Na/K+ ATPase pump, promotes calcium
Direct suppression of AV node conduction
Monitor digoxin levels
Sotalol 80mg PO TID Class III, prolongs action potential duration
130 Reference Material Reference Material 131
Diuretics
Drug Usual Dose Misc Info
Loop diuretics
Furosemide (Lasix) 10-100mg QID Needs k+ replacement
Bumex 0.5-10mg daily Needs k+ replacement
If not responding to high dose Lasix, consider
switching to Bumex
Thiazides
HCTZ (Hydrodiuril) 50-100mg qD
Chlorothiazide (Diuril) 500mg IV qD
Metolazone
(Zaroxolyn)
5-20mg qD
Potassium sparing:
Eplerenone (Inspra) 25-50mg qD
Spironolactone
(Aldactone)
25mg qD
Carbonic Anhydrase Inhibitor
Acetazolamide
(Diamox)
250-500mg IV q6h Increased renal excretion of bicarbonate (used in
metabolic/contraction alkalosis)
Bojar, R.M. (2011) Manual of perioperative care in adult cardiac surgery. (5th Edition).
POST-OP: DIAGNOSIS TRANSLATION EXAMPLES
Diagnosis Translation Examples
When documenting: Consider:
NPO, tube feeding, TPN, nutrition note:
diagnosis doc
Severe protein-calorie malnutrition, underweight
Altered mental status, Delirium Encephalophathy, type: acute delirium and etiology/cause
Chest pain Cause of chest pain, CHF, MI, CAD
CHF, ESHD Acuity and type of CHF
Myocardial infarction NSTEMI, STEMI (artery involved)
Hgb 7.5; 1L EBL, 2U PRBC given Acute blood loss anemia
Elevated BUN/Creatinine Acute Kidney Injury and or/ ATN
NA 125/150 with monitor and/or treatment Hyponatremia/Hypernatremia
5,3”, 297 lbs BMI > 40, Morbid obesity, overweight
WBC: 2.0, RBC 2.50, Plt: 75, on chemo Pancytopenia due to chemo
Hypoxia, Hypoxic, Hypercapnic Respiratory Failure (Acuity and Type)
Urosepsis, Meeting 2 out of 4 SIRS criteria Sepsis due to UTI
Pneumonia Pneumonia, specify etiology and/or causative organism
Fever Link cause of fever
Hypotensive require vasoactive drugs Shock and Type of Shock (Cardiogenic, Hypovolemic, post op, etc)
POST-OP: IICU ADMISSION REQUIREMENTS
iICU Admission Criteria
IV infusions
(patient must
have 3 or less)
Dopamine: max rate 10 mcg/kg/min via central line
Milrinone 0.375mcg/kg/min max
Amiodarone: central line administration strongly
preferred. Therapy via PIV for 24 hours max.
Argatroban, heparin
Insulin continuous infusion
Diltiazem
Ketamine
Esmolol (D1, CSU, B2 only)
Labetolol
Nitroglycerin (for controlling chest pain, 1 hour max)
Temporary
Pacemakers
Semi-Permanent Pacemakers
“Floating lead”, Transvenous – not allowed
“Fixed lead”, with external generator- allowed
Underlying rhythm/rate irrelevant
Temporary Epicardial Wires
If patient is pacer dependent, underlying heart
rate must be > 40 and be hemodynamically stable
CPAP/BiPAP
Nasal CPAP & BIPAP for patients established on a
nighttime CPAP/BiPAP (nasal mask) at home for OSA
Nasal CPAP & BIPAP as a new therapy for respiratory
evaluation and for a maximum duration of 4 hours.
Requires consultation of ICU team
Full face mask CPAP & BiPAP for patients with OSA is
permitted if treatment is an established home therapy and
patient is able to remove mask
High Flow
Nasal Cannula
HFNC can be accepted once patients are on stable
Patient must be evaluated every 4 hours for increasing
oxygen requirements
Pericardial
Drains
All Allowed
Post Cath
procedure
patients
Fast Track TAVRS
Post cardiac cath
132 Reference Material Reference Material 133
POST-OP: INR GOALS
Bioprosthetic
Aortic Valve
Bioprosthetic Mitral
Valve Replacement
Mechanical Aortic
Composite Valve
Mechanical Aortic
Valve Standard
Mechanical Mitral
Valve
Trans-catheter
Aortic Valve
Replacement
Atrial Fibrillation
Only
VTE Prophylaxis
INR Range (Goal) 1.5-2.5 2.0-3.0 2.5-3.5 (3.0) 2.0-3.0
Level of Evidence B B B B
Size of Treatment
Class I Class I Class I Class I
Duration Lifelong VKA Lifelong VKA Lifelong VKA
Level of Evidence A A A
Post-op
Anticoagulation
surgery once post-
operative bleed no
longer an issue.
(No bridge with
Heparin)
surgery once post-
operative bleed no
longer an issue.
(No bridge with
Heparin)
surgery once post-
operative bleed
no longer an issue.
(Bridge with
Heparin Post Op
24-36 Hours)
Dual antiplatelet
with clopidogrel
75mg for 6 months
if not on Coumadin
Unfractionated
Heparin 5000 Units
Subcutaneously
every 8 hours
unless patient is
bleeding (100 cc
per hour or more)
from Chest tubes
ASA Y/N (dose) Y (81-325mg) Y (75-100mg) Y (75-100mg) Y (75-100mg) Y (75-100mg) Y (75-100mg) -
lifelong
(75mg-325mg)
Level of Evidence B A A A C
Size of Treatment
Class IIa Class I Class I Class I Class IIb
HITT = heparin induced thrombocytopenia thrombosis
TIPS FOR CARDIAC SURGERY (Blue/Green) ANTICOAGULATION
*If patient has more than one indication for Coumadin use the highest
INR goal.
IF MECHANICAL MVR: patients should be started on heparin/argatroban drip
postop day 1 if no bleeding for bridging to Coumadin.
IF TEMPORARY PACING WIRES ARE STILL IN: DO NOT LET INR GET ABOVE 2.0
UNTIL THEY ARE REMOVED. Stay on heparin/argatroban drip until pacing wires
removed.
Heparin/Argatroban drip needs to be stopped for 6 hours prior to pacing wire
IF STARTING OTHER ANTICOAGULANTS (like Xarelto, Eliquis, Pradaxa, etc.) DO
NOT START UNTIL TEMPORARY PACING WIRES ARE REMOVED. IF indicated, use
heparin/argatroban drip until pacing wires are removed if indicated.
If on multiple blood thinning agents (ie Aspirin, Plavix, and Coumadin), discuss
with Cardiac Surgery that this is okay.
All patients are treated if blood test for HIT is positive, whether symptomatic or
not. Length of therapy should depend on Hematologist’s recommendation.
*Additional risk factors for thromboembolic events (AF, previous thromboembolism, LV
dysfunction, or hypercoagulable state) or an older-generation mechanical AVR (such as
ball-in-cage).
§ It is recommended to not start VKA until platelets have substantially recovered (i.e.,
usually to at least 150X109/L). VKA should initially be given in low doses (maximum,
5 mg of warfarin) over using higher doses (Grade 1C). If VKA has already been started
when diagnosed with HIT, vitamin K should be administered (Grade 2C). VKA should be
overlapped with a nonheparin anticoagulant for a minimum of 5 days and until the INR is
within target range (Grade 1C).
1) Guyatt GH, Akl EA, Crowther M, et al. American College of Chest Physicians Antithrombotic
Therapy and Prevention of Thrombosis Panel. Executive summary: antithrombotic Therapy
and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based
Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):7S-47S.
2) January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management
of Patients With Atrial Fibrillation: Executive Summary: A Report of the American College
of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart
Rhythm Society. J Am Coll Cardiol. 2014 Mar 28. Pii:S0735-1097(14)01739-2.
3) Kearon C, Akl E, Comerota A, et al. Antithrombotic therapy for VTE disease: Antithrombotic
Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians
Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb; 141 (2 Suppl):e419S-94S.
4) Linkins LA, Dans AL, Moores LK, et al. Treatment and prevention of heparin-induced
thrombocytopenia: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American
College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;
141(2suppl):e495s-530S.
5) Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of
patients with valvular heart disease; a report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines. J Thorac Cardiovas Surg. 2014 Jul;
148(1):e1-e132.
134 Reference Material Reference Material 135
POST-OP: PROPHYLACTIC MEDICATIONS
(GI, VA-PNA, DVT, INFECTION)
Common Prophylactic Medications
Pre Op
(day of surgery)
ICU iICU
VA- PNA
• Peridex 0.12%, 15mL
swish and spit
• Peridex 0.12%, 15mL swish and spit
while intubated
• N/A
DVT
• No DVT prophylaxis
indicated
• SCDs
• Heparin 5000 units subQ q8 hours
• SCDs
• Consider subq
Heparin if not able
to ambulate
Surgical
Prophylaxis
• 2g cefazolin
(3g if >120kg)
• Weight dosed
vancomycin if PCN
allergy
• Antimicrobial shower
x2 (PM and AM) before
surgery with either
chlorhexidine sponges
(per patient) or wipes
(per nurse)
• 2g cefazolin (3g if >120kg) x 3 doses
(24 hours)
• Weight dosed vancomycin if PCN
allergy x2 doses (24 hours)
• N/A
Lumbar
Drain
placed
drain in place
• N/A
GI
• N/A • IV or PO acid suppression therapy for:
o Mechanical ventilation > 48 hours
o Plt count < 50, INR > 1.5, or PTT 2x
baseline
o Spinal cord injury
o Solid organ transplantation
perioperatively in the ICU setting
o Use of two antiplatelet agents
o Any two of the following: Sepsis,
ICU stay > 10 days, occult bleeding
lasting > 6 days, high dose steroids
*Steroid use with no other risk factors
and NPO status are NOT indications for
stress ulcer prophylaxis
• Acid suppression
therapy only if
patient previously
took at home for
GERD
• Literature DOES
NOT support stress
ulcer prophylaxis
outside of the ICU
environment
POST-OP: SUPPLEMENTAL O2 & VENTILATOR
MANAGEMENT
Oxygen Administration
1. Nasal cannula
a.
i. FiO2 = 20% + (4 x O2 L/min)
b.
2. Face mask
a.
to determine an accurate FiO2 delivery since 75% of inspired volume is
room air
3. Venti mask
a. Delivers a precise oxygen concentration in increments of 24, 28, 31, 35,
and 40%
b. Inspired volume is a mix of room air and oxygen. Exhaled air is allowed to
exit the mask therefore CO2 retention is minimal
4. Non-rebreather mask
a.
b. There is a one way valve that prevents the patient from breathing in room
air. This ensures that a high oxygen concentration is delivered. Risk of
CO2 retention
5.
hypoxemia
a. FiO2 range 20-100%, Flow range 20-50 L/min
b.
Consider transitioning to regular nasal cannula once FiO2 weaned to 40-
Non-Invasive Positive Pressure Ventilation (NIPPV)
1. Continuous Positive Airway Pressure (CPAP)
a. Noninvasive ventilation mode that delivers positive pressure throughout
the respiratory cycle through specialized face or nasal masks
b. Prescriber must specify PEEP and FiO2
2. Bilevel Positive Airway Pressure (Bipap)
a. Noninvasive ventilation mode that delivers
b. Prescriber must set end-expiratory pressure (EPAP or PEEP) and IPAP
c. If Bipap is delivered using Drager or LTV vent, the ordered PS is additive
to the level of PEEP. i.e. PS 10 cmH2O & PEEP 5 cmH2O will deliver a total
IPAP of 15cmH2O
d. PS is not an additive to PEEP on Respironics Vision and V-60 devices
e. Consider placing NG/OG tube if IPAP > 20 cm H2O
Ventilator Modes: the most frequently used modes in the CVICU are
VC-AC, VC-SIMV and PSV
1. Volume-Controlled Ventilation (VCV)
a. VCV is volume-limited and time-cycled.
b. Prescriber must set a desired tidal volume, respiratory rate
c. The vent will deliver the set VT with every breath (machine or patient
triggered). Airway pressure aka peak inspiratory pressure (PIP) will vary
based on lung mechanics (resistance/compliance)
d. Vent setting parameters
i. Minute ventilation 8-10 L/min
ii. Tidal Volume (VT) 8-10 mL/kg (< 6 mL/kg for ARDS)
iii. Plateau airway pressures < 30 cm H2O
2. Pressure-Controlled Ventilation (PCV)
a. PCV is pressure-limited and time-cycled.
b. Prescriber must set desired pressure limit, respiratory rate, and
inspiratory time (I:E ratio)
c.
pressure for the duration of the inspiratory time. VT will vary based on
lung mechanics
d. Vent setting parameters
i. Peak inspiratory pressure < 35 cm H2O
3. Assist Control Ventilation (ACV)
a. ACV can be either pressure or volume limited
b. The ventilator delivers the same set parameters for both mandatory and
patient triggered breaths.
136 Reference Material Reference Material 137
4. Synchronized Intermittent Mandatory Ventilation (SIMV)
a. Assisted breaths are synchronized to coincide with spontaneous
5. Pressure-Support Ventilation (PSV)
a.
b. The prescriber sets the pressure support level
c. Each breath is patient triggered and the tidal volume is determined by
6. Airway Pressure Release Ventilation (APRV)
a. Alternates between high/low airway pressure and is time-cycled (not
patient triggered). Most time is spent at high pressure with a brief cycle
to low pressure. Purpose of this type of ventilation is to keep alveoli
recruited
7. Inverse Ratio Ventilation (IRV)
a. This mode of ventilation uses a prolonged inspiratory time (2:1) in
order to help prevent alveolar collapse. May be used for patients
with refractory hypoxemia with conventional modes of ventilation.
PEEP: Peak end expiratory pressure
1. Therapeutic Uses:
a. Patients admitted to ICU on ventilator will be set on PEEP 5cm H20
i. PEEP 5 considered a substitute for loss of normal breathing
“Physiologic PEEP” caused by the presence of the ETT (endotracheal
tube)
ii. Usually well tolerated hemodynamically, not much recruitment/O2
b. Increasing PEEP to increase PaO2
i. Increasing PEEP (by 2-5cm H20 increments) will increase mean airway
pressure and open previously closed alveoli
ii. Increases lung surface area participating in gas exchange
iii. Decreases VQ/intrapulmonary shunting by improving ventilation to
perfused lung
iv. As lung recruitment and PaO2 improves, FiO2 may be weaned
c. Cautions with high PEEP
i. Increased intrathoracic pressure decreases venous return to the heart
ii. Increased PEEP leads to increased PVR, leading to more strain on RV
iii. Decreased venous return and depressed RV performance may lead to
iv. Should not be used in patients with COPD (leads to increased VQ
mismatch)
v. Monitor for signs of “barotrauma:”
1. Caused by alveolar overdistention
2. May present as: pneumothorax, subcutaneous emphysema,
pneumomediastinum
Lung Mechanics
1. End-inspiratory Peak pressure
a.
the airways, and elasticity of lungs and chest wall
2. End-inspiratory Plateau pressure
a. Pplat is a direct measurement of the elasticity of the lungs and chest wall
(compliance)
b.
3. Tips
a. If peak pressure is elevated and plateau pressure is unchanged, there is
an increased resistance in the airways which may be due to secretions in
the ETT, mucous plug, or acute bronchospasm
b. If both peak and plateau pressures are elevated, there is decreased
compliance of the lungs and/or chest wall. Causes may include
pneumothorax, atelectasis, acute pulmonary edema, worsening
pneumonia, or ARDS
c. If peak pressure is decreased, there is a problem with an air leak in the
ventilator system
d. PEEP increases plateau pressure
CV-ICU Interdisciplinary Rapid Extubation Protocol (I-REP)
1. Assess patient to determine if patient meets vent weaning criteria
a. Weaning criteria:
i. SpO2 > 92% on FiO2 < 60%
ii. PEEP < 8 cm H2O
iii. Temp > 35C
iv. Hemodynamically stable
v. Chest tube output stable
vi. Spontaneous breathing noted (if patient not over-breathing,
then reduce respiratory rate by 50% for up to 5 min to assess for
spontaneous breathing)
2. If patient meets weaning criteria then reduce respiratory rate to zero as
tolerated while maintaining EtCO2 < 50.
a. Goal PSV - PS 10, PEEP 5, and normal work of breathing with RSBI < 100
3. If patient does not tolerate PSV, return to previous vent settings and reassess
4. If tolerates PSV, check ABG and assess neuro to see if patient meets
extubation criteria.
a. Extubation criteria
i. SpO2 > 92% on FiO2 < 50%
ii. EtCO2 stable and within baseline +/- 10%
iii. pH > 7.3
iv. PS 10 and PEEP 5
v. RSBI < 100 with normal work of breathing
vi. If patient does not meet criteria, reassess every 15 min for a total of 3
cycles
5. If extubation criteria are met, then ok to extubate. If patient is morbidly obese
or has a h/o OSA then extubate to CPAP 8-10 cm or Bipap 10/5 for 2 hours
6. If patient is receiving inhaled Flolan, extubate to HFNC to continue Flolan
administration
Miscellaneous
1. Do not change any ventilator settings unless in an emergency. Please notify
respiratory therapy team for all ventilator changes
2. Rapid-shallow breathing index (RBSI) = RR / Liters of Tidal Volume
a. Goal RSBI < 100
b. Indicator for appropriateness for extubation (along with mental status,
amount of secretions, strength of cough, etc)
3. Indirect Calorimetry
a. Nutrition is important because too few calories causes respiratory muscle
catabolism and muscle weakness. Too many calories (particularly carbs)
increases metabolic rate and can result in respiratory muscle fatigue or
hypercapnia due to increased CO2 production
b. b. Indirect calorimetry is a measurement of resting energy expenditure
based on oxygen consumption (VO2) and carbon dioxide production (VCO2)
138 Reference Material Reference Material 139
POST-OP: VAD BOWEL REGIMEN PROTOCOL
Standards of Practice for VAD patients to reduce Post-po Ileus
VAD Quality Improvement
Vincenta M. Grassano, RD, CNSC
Heart Failure Service/D1
1. Initiate bowel regimen the day of admission (Pre-op)
a. Senna 2 tabs BID
b. Docusate 100mg BID
2. Escalate bowel regimen if no BM within 24 hours of surgery
a. Bisacodyl 10mg per rectum x1 occurrence
b. Magnesium Citrate 300mL x1 occurrence (not for patients with renal
dysfunction)
c. Check potassium and magnesium
3. Adhere to Pre-Op diet regimen
a. Patient to receive diet order for recommended PO Diet or TF
(carbohydrate containing meal) up to 24 hours before surgery
b. MD order for Liquid Diet (carbohydrate containing liquids ie juice or
Ensure clear) up to 6 hours prior to surgery rather than NPO
c. Patient to be NPO 6 hours prior to surgery
CVICU Service / Immediate Post-op
1. Resume bowel regimen POD #0
a. Senna syrup 10mL via feeding tube BID
b. Increase docusate solution 200mg via feeding tube BID
c. Add Miralax 1 packet BID
d. Bisacodyl 10mg per rectum daily
2. Keofeed placed if unable to extubate by POD #2
a. Allows for early nutrition
b. Allows for immediate administration of bowel regimen/medications
3. Initiation of Nutrition by POD #2
(with the potential to meet estimated needs)
a. If intubated initiate tube feeds
b. Initiate Full liquid or Regular diet (sugar free clear liquid and clear liquid
diet do not have potential to meet estimated needs)
c. Supplements if needed
4. Escalate bowel regimen POD #4 if no bowel movement or atus
a. Lactulose 20mg TID (NOTE: can cause abdominal discomfort and
cramping)
b. Either:
i. Mineral oil enema
ii. Magnesium citrate (150-300mL) *(not for patients with renal
dysfunction)
5. KUB POD #5 if no BM of Flatus
6. Taper down regimen if multiple bowel movements s/p bowel regimen
a. Docusate solution/capsule 200mg BID: continue as scheduled
b. Senna syrup 10mg BID: change scheduled to PRN
c. Miralax 1 packet BID: change scheduled to PRN
POST-OP: END OF LIFE CARE
Use these guidelines to transition a patient to comfort care and
perform discharge as deceased documentation
1. Family, patient (if able), ICU team and surgical team agree to withdraw care
2. Discontinue all orders in Epic (including medications, labs, nursing care
orders, etc)
3. Order the IP ICU End of Life Order Set (#1791) in Epic
a. Choose the appropriate analgesics and anxiolytics as discussed with ICU
attending
b. Order the Comfort Care code status within the order set
4. Work with the ICU Attending, bedside nurse and respiratory care to determine
the sequence of support withdrawal
5. Work with the resource/charge RN to have Chaplain services available
6. Resource/charge nurse will notify the Transplant Donor Network
7. Once the patient has passed, you or another licensed provider should
examine the patient and declare Time of Death
a. Make note of this time, you will use it multiple times in documentation
b. You or the ICU attending should approach the next of kin about autopsy
request
8. Discharge as Deceased Documentation
a. Use the Discharge Navigator and choose the “Discharge as Deceased” tab
located at the top of the Discharge Navigator
b. Fill in the Death Certicate Worksheet by selecting “New Reading” and
i. This will be used by Chaplain services to complete the Death
ii. Call the Coroner (408-793-1900) to report the death
1. They will ask you the patient’s address (located in Demographics)
2. They will ask Cause of Death and brief synopsis of what happened
3. Document the case/release number and the name of the person
you talked to in the appropriate space in Epic
iii. Complete the “Cause of Death” Documentation
1. “Cardiopulmonary arrest” is Not a viable diagnosis
2. When in doubt, ask the ICU attending what to list
c. Complete the Deceased Summary within the navigator
ii. Select the ICU Attending as the cosigner
d. Complete the Discharge Summary
ii. Delete non-applicable sections as needed
iii. Same information as the Deceased Summary, may copy-paste
iv. List the Surgical attending as the cosigner
9. Write the Discharge Order
a. Disposition: Deceased
140 Reference Material Reference Material 141
POST-OP: PATIENT PROGRESSION CHECKLIST
Patient Progression Towards Discharge
Pain- well controlled with oral meds
Remove OnQ (Bupivicaine pump) 1 day prior to discharge))
Remove devices (Chest tubes, Pacer wires, Foley, A-line)
Transition to PO Medications
ASA, statin
Beta-Blocker if applicable
Need for Anticoagulation? Transition to PO anticoagulants
Adequate diuresis? Transition to PO diuretics
Do any medications require prior authorization? (Consult with Case
manager)
Commonly prescribed medications requiring prior authorization
include: NOAC (Eliquis, xarelto), oxycontin
Tolerating diet, BM since surgery
Post-operative imaging (consult with chief resident/surgical attending)
CT scan +/- Echo (surgeon and operation dependent)
2-view CXR (done in radiology suite) at dry weight prior to discharge
PT eval: Home vs. home with home health therapy vs. Skilled Nursing Facility
Consult with E-29 Case Manager to start referral process if needed
Contact: 650-847-7453 (work cell-phone)
Cardiac rehab: Discharge teaching
Cardia Rehab ghost pager: 1-5736
Establish follow up appointments with Nurse Coordinator (PCP, Cardiologist,
INR clinic, etc). Contact via cell-phone:
Dr. Boyd, Dr. Ha: Sally Eastman 650-627-6373
Dr. Woo: Ashley Liang 650-683-0114
Dr. Lee, Dr. Hiesinger: Pres Lorenzo 650-850-2828
Dr. Fischbein, Miller: Judi Lachenmyer 650-498-7731 (ext 87731)
NOTES
142 Reference Material Reference Material 143
NOTES NOTES
144 Reference Material
DEPARTMENT OF CARDIOTHORACIC
SURGERY HANDBOOK—VERSION II
Faculty Advisors:
Y. Joseph Woo, MD
Jack H. Boyd, MD
Charles Hill, MD
Charlene Kell, EMBA, BSN, RN, CCRN, FACHE, NEA-BC
Anson M. Lee, MD
Kapilkumar N. Patel, MD
Contributing Authors:
Scarlette Aliga-Cabamungan, MS, RN, AGACNP-BC
Irina Axelrod, PA-C
Christopher J. Bilbao, DO
Sarah Booth, ACNPC-AG, MSN, CCRN
Zoe Chan, PA-C
Kristie Duoss, MSN, ACNP-BC
Clara George, NP
Hilary C. Hammond, MMS, PA-C
Christine Hartley, RN, MS, ACNP-BC
Aleya Hyderi, PA-C
Kelly Juarez, MPAS, PA-C
Yukfung Lee, PA-C
Xin Ma, MMS, PA-C
Erica Mikhli, PA-C
Shari Miller, PA-C, FAPACVS
Mykl Morrissey, MSN, RN, AGACNP-BC
Richard Quitevis, MS, RN, AGACNP-BC
Hardeep Reddick, MBA, PA-C
Suzanne Sewell, MSN, RN, FNP-BC
Joe Simmons, MS,ACNP-BC
Tim Shieh, PA-C
Y. Kevin Zeng, MS, AGACNP-BC, RN
Contributing Editors:
Megan Atashroo, MSN, RN-FA, FNP-BC
Mary Sheridan Bilbao, MPAS, PA-C, FAPACVS
Corinne Pogemiller, MMSc, PA-C
Emily Tognozzi, MMS, PA-C
Disclaimers:
Although care has been taken to ensure the accuracy of content of this
handbook, it should not be a substitute for clinical judgment. Neither the
authors nor editors assume any liability for injuries and or damage related to this
publication.
For internal use only, not for sale or re-distribution. Use for intended audience
only. Not for patient education.
